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The tongue - evidence of intelligent design

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1 The tongue - evidence of intelligent design on Fri Jul 07, 2017 4:54 am

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The tongue - evidence of intelligent design

http://reasonandscience.heavenforum.org/t2579-the-tongue-evidence-of-intelligent-design

Some interesting facts about taste and tongues:

Of all the types of microbes living in your mouth, bacteria are the most numerous. It has been estimated that there are over 100 million in every millilitre of saliva from more than 600 different species. The mouth is one the more dangerous places in the human body in terms of what comes out, what goes in, and what lives there. Fungi, micro-organisms, and viruses constantly come in with every bite of food and frequently just from breathing. In spite of all that, the tongue rarely gets infected, and when it does, it usually heals quickly. One reason is that the tongue secretes an antibiotic called “lingual antimicrobial peptide.” Studies done at the Magainin Research Institute show that the tongue secretes more antibiotic when there is a sore or injury. Our bodies are designed to survive in a world that has all kinds of things that could do us harm. The tongue is only one small, but important example of how design protects us from the dangers around us.

The woodpecker’s tongue is even more amazing than the headache-proof crash helmet it wears. Darwinists call it an “adaptation” which means it just happened that way because woodpeckers wanted to eat beetle larvae way inside trees–and were willing to wait a million years or so for their tongues to grow long enough to reach them. They say what proves it is an adaptation is that woodpecker tongues are just like other bird tongues, only longer (at least three to five times the length of its beak in some species)–as if two objects that are similar in some way have to be descended from a common ancestor rather than having been molded by a common Artist. Actually, unlike other birds, the tongue of a woodpecker is not attached to the rear of its mouth. And, unlike any other tongues, it apparently doesn’t stay attached in one place. To get a meal, the woodpecker buttresses its tail against a tree trunk, forming a tripod with its toes (two in front, two in back) and listens. Once it has determined that beetles are scuttling around inside and has drilled a hole with its beak, the base of its tongue disengages from under the jaw and re-attaches between its eyes as it plays out. The tongue is sensitive enough to feel the softness of a larval insect, yet stiff and sharp enough to pierce it (other studies indicate it is flexible and actually wraps around its prey) and sticky, with reverse barbs to keep the grub on the tongue as it retracts.

Hummingbird tongues are elastic micropumps
Pumping is a vital natural process, imitated by humans for thousands of years. We demonstrate that a hitherto undocumented mechanism of fluid transport pumps nectar onto the hummingbird tongue. Hummingbird tongues pick up a liquid, calorie-dense food that cannot be grasped, a physical challenge that has long inspired the study of nectar-transport mechanics. Existing biophysical models predict optimal hummingbird foraging on the basis of equations that assume that fluid rises through the tongue in the same way as through capillary tubes. We demonstrate that the hummingbird tongue does not function like a pair of tiny, static tubes drawing up floral nectar via capillary action. Instead, we show that the tongue tip is a dynamic liquid-trapping device that changes configuration and shape dramatically as it moves in and out of fluids. We also show that the tongue–fluid interactions are identical in both living and dead birds, demonstrating that this mechanism is a function of the tongue structure itself, and therefore highly efficient because no energy expenditure by the bird is required to drive the opening and closing of the trap. Our results rule out previous conclusions from capillarity-based models of nectar feeding and highlight the necessity of developing a new biophysical model for nectar intake in hummingbirds. Our findings have ramifications for the study of feeding mechanics in other nectarivorous birds, and for the understanding of the evolution of nectarivory in general. We propose a conceptual mechanical explanation for this unique fluid-trapping capacity, with far-reaching practical applications (e.g., biomimetics).

Blue whale tongues weigh almost 6,000 pounds. That's as much as African forest elephants weigh! They probably use their giant tongues to pick some of the thousands of pounds of krill out of their toothbrush bristle-looking baleen plates. Some snakes use folds of skin in their mouths to soak up water like a sponge through a mechanism called capillary action, a 2012 study found. Pangolins, a relative of anteaters, have long, sticky tongues supplied by an overactive salivary gland that they use to eat thousands of ants. The mammals are hunted in parts of Asia for their meat and scales, and are critically endangered. The okapi, which is related to giraffes and looks kind of like a zebra, has a tongue so long it can lick its own eyes and ears. The animal uses its lengthy tongue to strip leaves off of trees and into its mouth. Dogs make little cups out of their tongues when they drink water, and they are much sloppier than cats. Cat tongues make cups, too. Felines create a column of water under their tongue when they elegantly place it on the surface of the liquid. Mesmerizing, isn't it? Mallee fowl don’t sit on their eggs, like most birds do to let their body heat incubate the eggs. They build a large mound and monitor its temperature with their bill and tongue. The hen usually begins laying in late September — the southern hemisphere spring. From that time until about April, the male uses his beak and tongue to ensure that the temperature of the mound stays constant.

Chameleon Tongues
The chameleon also has one of the fastest tongues on the planet. It is so fast, in fact, that it is difficult for the human eye to see it when the lizard shoots it at potential prey (which may be more than a body length away). Just how fast is this super-hero-like tongue? Scientists have discovered that the chameleon’s tongue can accelerate five times faster than a fighter jet. Now that is fast! The design we see in nature is powerful evidence for the existence of God. Indeed, it is so powerful that it forced world-renowned atheist Antony Flew to admit his lifetime of scholarship was wrong and that God must exist. The more we learn about this planet and the life on it, the more we stand in awe of that amazing design. The chameleon is an excellent example of this trend. For a long time, scientists have known about the amazing design features of the chameleon. The more we learn, however, the more amazing chameleons become! Chameleons’ long, elastic tongues are one of the fastest muscles in the animal kingdom, extending more than twice their body length and packing 14,000 watts of power per kilo. But it is the smallest species that strike fastest, according to a new study. Researchers filmed tongue strikes of chameleons attacking a suspended cricket, at 3000 frames per second. They found that the animals’ tongues are capable of impressive acceleration, doing 0 kilometers to 100 kilometers per hour in one-hundredth of a second, twice as fast as the fastest car. And, like sports cars, the smallest chameleons are the most powerful. Across 20 species, ranging from the tiny 1-cm rosette-nosed chameleon (Rhampholeon spinosus) to the half-meter Malagasy giant chameleon (Furcifer oustaleti), the team found that smaller species’ tongues could accelerate at more than 250 g, five times faster than that of the largest chameleon. This is because small chameleons have evolved larger tongues relative to their body size, handy since they also need to consume proportionally more food to survive. As well as raw muscle power, chameleons spring-load the elastic tissue in their tongue, catapulting it toward prey when they strike, and giving them the highest acceleration and power output of any reptile, bird, or mammal. Previous studies underestimated their power because they failed to consider the little guy.

Salamander Tongue Is World's Most Explosive Muscle
The greatest burst of power from any animal muscle comes from the tongue of a tropical salamander, scientists have announced. The giant palm salamander of Central America (Bolitoglossa dofleini) captures fast-moving bugs with an explosive tongue thrust that releases over 18,000 watts of power per kilogram of muscle. 8 The salamander's ballistic firing permits the tongue's sticky-padded tip to reach prey in just a few thousandths of a second. Deban noted that the greatest power output from muscle acting alone has been measured in quail as they flap their wings in vertical takeoff.

The sticky, elastic tongues of amphibians have fascinated researchers for decades—the first study of frog and toad tongues was done in 1849. However, the underlying physics of this adhesive feat remained unclear. Previous studies compared frog tongues to scotch tape, but that’s not the full picture, researchers report today in the Journal of the Royal Society Interface. Yes, frog tongues are uniquely sticky (and their saliva makeup is crucial in bug capture), but they’re also very soft—10 times softer than human tongues and one of the softest known biological materials. That softness makes frog tongues more like adhesive shock absorbers than scotch tape, the researchers suggest. Here’s what happens: Say a bug is buzzing by and a frog releases its tongue. When the bug hits the frog’s tongue, the tongue wraps around the bug like a sticky bubble gum blanket and absorbs the bug’s inertia. Upon impact, the bug gets coated in saliva. Because the tongue is so soft, it can stretch out more than twice its thickness to cover more of the bug’s surface area and get its saliva into the grooves of a bug’s bumpy exoskeleton. Frog saliva is a non-Newtonian fluid, the team found, meaning it defies Newton’s law of viscosity and its flow changes under stress. So the saliva flows normally until the bug hits it, and then the saliva grips the bug as the tongue is retracted back into the frog’s mouth. But if a frog’s tongue is so sticky, how does it get its meal off its tongue and into its stomach? In a much studied phenomenon, frogs swallow with their eyes. The researchers found that when the eyes push against the bug in a motion parallel to the tongue, the saliva starts to flow easily again and down goes dinner. And although the researchers no longer think frog tongues are all that similar to scotch tape, this new finding might help them design new adhesives that stick at high speeds.

Flamingo Tongues Are Weirdly Phallic
There are a couple things that make flamingo tongues way weirder than average. First are the spiny bristles that coat their tongues, an adaptation that allows them to filter their food much like baleen whales do. On top of these unusual spines, scientists have discovered erectile tissue. These are a crucial part in how flamingo tongues work. When feeding, this tissue will fill with blood and become rigid. Since flamingos feed by dipping their heads upside down in water, researchers hypothesize this swollen tissue assists in the stabilization of their heads.



How vertebrates switched from feeding via suction to evolve a tongue remains unclear. 14

Taste perception: from the tongue to the testis 15
In mammals, the sense of taste helps in the evaluation and consumption of nutrients, and in avoiding toxic substances and indigestible materials. Distinct cell types expressing unique receptors detect each of the five basic tastes: salty, sour, bitter, sweet and umami. The latter three tastes are detected by two distinct families of G protein-coupled receptors: T2Rs and T1Rs. Interestingly, these taste receptors have been found in tissues other than the tongue, such as the digestive system, respiratory system, brain, testis and spermatozoa. The functional implications of taste receptors distributed throughout the body are unknown. We therefore reviewed the remarkable advances in our understanding of the molecular basis of taste perception in ‘taste’ and ‘non-taste’ tissues. We also present our speculations on the direction of further research in the field of male reproduction.

The anatomical substrates and units of taste detection are the taste receptor cells (TRCs), which are assembled into the taste buds distributed on the epithelium of the tongue and palate. Theoretically, the basic taste sensations are each recognized by different cells that express specialized receptors and distinct transduction pathways . Sour and salty tastes modulate the function of TRCs by the direct activation of specialized membrane channels.  In contrast, sweet, bitter and umami taste transduction is mediated by a common G protein-coupled receptor (GPCR) signalling pathway.

Taste signal transduction
In general, the following molecular model has been suggested for signal transduction by taste receptors. When a tastant binds to T1Rs or T2Rs, taste GPCRs activate the heterotrimeric G protein α-gustducin. Ligand binding results in the release of the Gβγ13 subunits and the subsequent stimulation of phospholipase C-β2 (PLCβ2). Activation of PLCβ2 hydrolyses phosphatidylinositol-4,5-bisphosphate to produce two intracellular messengers, inositol-1,4,5-trisphosphate and diacylglycerol, and ultimately leads to calcium release from internal stores and activation of the taste transduction channel (the transient receptor potential protein, TRPM5;

The receptors and cells for mammalian taste  16









The receptor cells for taste are modified epithelial cells organized into taste buds, which are scattered on the tongue.
Binding of a sugar molecule to a receptor cell initiates a signal transduction pathway.
Sodium channels open, Na+ ions diffuse into the cell, and the membrane depolarizes.
Nerve signals are then sent to the parietal lobe of the cerebrum. 17


Mouth Bacteria 12
Of all the types of microbes living in your mouth, bacteria are the most numerous. It has been estimated that there are over 100 million in every millilitre of saliva from more than 600 different species. 

Antibiotic Tongue 1
The mouth is one the more dangerous places in the human body in terms of what comes out, what goes in, and what lives there. Fungi, micro-organisms, and viruses constantly come in with every bite of food and frequently just from breathing. In spite of all that, the tongue rarely gets infected, and when it does, it usually heals quickly.
One reason is that the tongue secretes an antibiotic called “lingual antimicrobial peptide.” Studies done at the Magainin Research Institute show that the tongue secretes more antibiotic when there is a sore or injury.
Our bodies are designed to survive in a world that has all kinds of things that could do us harm. The tongue is only one small, but important example of how design protects us from the dangers around us.

1. The tongue is the only muscle in human body that works without any support from the skeleton 13
2. Our tongue is the home of our taste buds. When looked under a magnifying glass, hundreds and thousands of small bumps will become visible on the tongue. These bumps are known as papillae and are the actual home of our taste buds.
3. Tongue is not the only place where taste buds live. Taste buds can also be found on the inside of our cheeks, on lips, on the roof of our mouth and even under the tongue.
4. Approximately, there are 10,000 taste buds in our mouth of which 8,000 live on our tongue and the remaining 2,000 are found in the places we mentioned in the previous point.
5. There are specific segments on tongue for sensing different tastes. The notion that different parts of the tongue is responsible for sensing different types of tastes (in other words, there are taste belts) is actually a myth. Our tongue can taste sour, sweet, bitter, salty and umami. Umami is actually a very new variant of taste discovered by a Japanese scientist who found that the chemical that is responsible for this taste is monosodium glutamate.
6. Our tongue is the only muscle in our body that is capable of sensing taste and sending taste signals to the brain. Each individual taste bud has around 15 receptacles that are responsible for carrying taste signals to our brain.
7. The tongue is THE STRONGEST muscle in entire body. However, it is at the same time, one of THE MOST sensitive muscles as well.
8. In terms of flexibility, tongue beats every other muscle in our body! Because of this flexibility, the tongue is capable of easily manipulating food inside the mouth and is also capable of acting as a natural cleanser for our teeth after a meal.
9. Our tongue has a very unique property. It is incapable of detecting taste if it is dry. This means that if you place a piece of lemon on a dry tongue, you will not be able to tell that it is sour. The tongue gets its ability to sense taste only in the presence of saliva that keeps it moist.
10. The color of the tongue can tell a lot about a person’s health. Here are some color indications about health: Pink Tongue = Good Health; White Tongue = Fungal Infection and Yellow Tongue = Stomach Problem or Fever.
11. Tongueprints (actually tongue imprints) of humans are unique (very much same as the fingerprints). Tongues of different humans are of different shapes and will have different number of taste buds, thus making the tongue imprints unique.
12. Tongue has a really really rough texture. Did you ever notice that while kissing someone?
13. Women have shorter tongues compared to males.
14. We mentioned in point 9 that a dry tongue is incapable of detecting taste. That’s because taste buds are capable of sensing taste only when molecules of the food (or whatever you put in your mouth) dissolve in water (our saliva consists of water). This essentially means that you cannot sense taste of anything whose molecules do not dissolve in water even if you have a moist tongue. Ever tried tasting glass?
15. Here is an interesting tongue fact – you don’t keep your tongue clean and you will get bad breath. Why so? That’s because our mouth is the home of 600 different types of bacteria and a single saliva drop contains 1 million of those bacteria. Our entire tongue remains moist due to saliva. So, can you ever imagine the number of bacteria present on our tongue?
16. Every taste bud on our tongue has somewhere between 50 and 100 taste sensing cells. No individual cell is capable of tasting more than one taste.
17. About 2/3rd of the tongue is visible and the remaining 1/3rd is not visible. The part that is not visible is close to the throat.
18. In Tibet, you can merrily stick your tongue out at others. It will not be considered rude or childish. In Tibet, it is actually a greeting.
19. The tongue is more important than we think. It does not only help to taste food but also helps to talk, to spit, to swallow and even to kiss.
20. The longest human tongue to be ever recorded was 3.86 inches from back to tip. The widest tongue measured 3.1 inches. The longest female tongue to be ever recorded was 2.76 inches.

10




Woodpecker tongue 2
The woodpecker’s tongue is even more amazing than the headache-proof crash helmet it wears.
Darwinists call it an “adaptation” which means it just happened that way because woodpeckers wanted to eat beetle larvae way inside trees–and were willing to wait a million years or so for their tongues to grow long enough to reach them. They say what proves it is an adaptation is that woodpecker tongues are just like other bird tongues, only longer (at least three to five times the length of its beak in some species)–as if two objects that are similar in some way have to be descended from a common ancestor rather than having been molded by a common Artist. Actually, unlike other birds, the tongue of a woodpecker is not attached to the rear of its mouth. And, unlike any other tongues, it apparently doesn’t stay attached in one place. To get a meal, the woodpecker buttresses its tail against a tree trunk, forming a tripod with its toes (two in front, two in back) and listens. Once it has determined that beetles are scuttling around inside and has drilled a hole with its beak, the base of its tongue disengages from under the jaw and re-attaches between its eyes as it plays out.
The tongue is sensitive enough to feel the softness of a larval insect, yet stiff and sharp enough to pierce it (other studies indicate it is flexible and actually wraps around its prey) and sticky, with reverse barbs to keep the grub on the tongue as it retracts.



There’s the problem. You’re a woodpecker and you have a tongue three to five times as long as your beak. When you retract it, where does it go? Where can you store it? Can you wrap it around your brain or something? As a matter of fact, yes. When not in use, the European Green Woodpecker’s tongue goes “. . . around the back of the skull beneath the skin, and over the top between the eyes, terminating usually just below the eye socket.” Lane P. Lester and Raymond G. Bohlin, The Natural Limits to Biological Change (Grand Rapids: Zondervan, 1984), p. 25, 3

“In the case of the Red-bellied Woodpecker. . . the tongue forks in the throat, goes below the base of the jaw, and wraps behind and over the top of the head, where the forks rejoin and insert in the bird’s right nostril or around the eye socket.” 4

(Scientifically, “when the woodpecker wants to stick out its tongue, it contracts branchiomandibularis muscles near the base of the hyoid apparatus. This forces the hyoid bones forward within their sheath and propels the tongue out of the bill. Relaxing the muscles allows the tongue to shorten and brings it back inside.” Ibid.)

I would have loved to watch Blind Chance sittin’ there on the ground fumbling with woodpecker tongues (and butterfly wings and weeds and clam shells, whatever, since it can’t tell one from another), dropping one skull and picking up another and poking some things at other things, starting over with every single attempt (because it is too dumb to remember what it did last time and too dumb to know whether it worked or not so it can improve on it), suddenly coming up with something so creative even the biologists have to keep cautioning each other to “constantly keep in mind that what they see was not designed” (Francis Crick, Ph.D.). When Thomas Edison tried to find a filament that would work in a light bulb, he had the advantage of a brain and opposable thumbs and eyesight–not to mention foresight. It took him from 3,000-10,000 tries, depending on who you read. Can you imagine how many tries it took for Natural Selection to cobble together something so intricate and complicated? With maybe a fortunate mutation and a dab of genetic drift along the way, one random stab after another after another after another after another after another. . .



For years scientists have been trying to find out how the woodpecker avoids damaging its brain up against its skull as it slams its head into a tree at up to 20 ft/sec. 5
Unlike other animals like bighorn rams that butt their heads together, the woodpecker does not have a double bone in the front of the skull that acts like a shock absorber.  They only have a single layer of bone.  This has long intrigued scientists, so a team from the Hong Kong Polytechnic University led by Ming Shang set out to discover the woodpecker’s secrets.
They filmed a woodpecker in slow motion striking against a pressure plate to capture the details of the impact.  Upon careful examination of the slow motion footage, they discovered that the woodpecker turns its head just enough to lessen the effects of a direct impact. In addition to the slow motion studies, they also used computer thermal tomography of the skulls of woodpeckers.  This study revealed that there is a slight difference in the length of the upper and lower beaks.  The amount of force created at the tip of the beak is greater than the force that is transmitted to the bones of the skull.  It was determined that the difference in beak length served to reduce the force of impact.

They also used a scanning electron microscope to examine the bones of the skull.  Under the details of the microscope it was revealed that the bones in the front of the skull have what they described as a ‘spongy’ structure in key locations.  These spongy pockets are strategically placed so as to absorb some of the shock force.
The brain of the woodpecker is also shaped in such a way as to minimize the possibility of brain damage.  Instead of being longer front to back like the human brain, the woodpecker’s brain is longer up and down, thus reducing the impact surface and subsequent shock force.

If you have ever watched any kind of crime show or forensic program that involved someone being strangled, you probably heard reference to the hyoid bone.  In humans, this is a small horseshoe shaped bone that lies just over the Adam’s apple.  It is not connected to any other bone and is fairly fragile.  The hyoid is so thin that it is easily broken when someone is manually strangled. In the case of the woodpecker, the hyoid bone is much different.  According to the report I read the woodpecker’s hyoid acts like a safety belt and was described as: Starting at the underside of the birds’ beaks, it makes a full loop through their nostrils, under and around the back of their skulls, over the top and meeting again before the forehead. Other scientists are now looking at the design features of the woodpecker’s skull to see if it will help them create more efficient safety helmets for sports, and for bicyclists and motorcyclists.  I always have to smile when scientists spend so much effort and intelligence trying to duplicate what they believe happened by chance in nature.



What I found confusing in the report that I read was they attributed the woodpecker’s special features to only three things: the hyoid bone, the difference in length between upper and lower beaks and the spongy structures of the bones of the skull. However, when as I read their report, I counted five design features not three.  To their list you have to add the way the woodpecker turns its head at impact and the shape of the brain. When you add all of these features together, you get an extremely complex set of design features that all have to be in place in order for the woodpecker to avoid turning its brain into mush as it pecks against tree after tree.  If they evolved one feature at a time, the woodpecker would never have survived long enough to pass its traits on to subsequent generations. When talking about the special design features of the woodpecker’s skull, you also have to consider their tongue and how it sets in their head.  The woodpecker has a very long sticky tongue that is far too long to fit in its bill.  They use these long sticky tongues to pull insects out of the holes they drill into the trees. So if the tongues are too long to fit into the bill, where does it go? The tongue is pulled into a muscular sheath that extends under the scalp, around the head and then back into the right nostril.  I have yet to see an evolutionary explanation for this weird feature. Add the special design features listed above to the weird design of the tongue and you have far too many unique features that all needed to be in place for the woodpecker to survive.  So the next time you see or hear a woodpecker hammering away at a nearby tree, take the opportunity to share its unique designs with those with you.  Explain to them that the only possible explanation for the woodpecker is our all-knowing Creator God. 6

The Hummingbird Tongue 7
Hummingbird tongues pick up a liquid, calorie-dense food that cannot be grasped, a physical challenge that has long inspired the study of nectar-transport mechanics. Existing biophysical models predict optimal hummingbird foraging on the basis of equations that assume that fluid rises through the tongue in the same way as through capillary tubes. We demonstrate that the hummingbird tongue does not function like a pair of tiny, static tubes drawing up floral nectar via capillary action. Instead, we show that the tongue tip is a dynamic liquid-trapping device that changes configuration and shape dramatically as it moves in and out of fluids. We also show that the tongue–fluid interactions are identical in both living and dead birds, demonstrating that this mechanism is a function of the tongue structure itself, and therefore highly efficient because no energy expenditure by the bird is required to drive the opening and closing of the trap. Our results rule out previous conclusions from capillarity-based models of nectar feeding and highlight the necessity of developing a new biophysical model for nectar intake in hummingbirds. Our findings have ramifications for the study of feeding mechanics in other nectarivorous birds, and for the understanding of the evolution of nectarivory in general. We propose a conceptual mechanical explanation for this unique fluid-trapping capacity, with far-reaching practical applications (e.g., biomimetics).


Fig. 1.
Hummingbird tongues. (A) Nectarivores use their tongue (yellow) as their primary food-gathering tool. (B) Lateral picture of a post mortem Ruby-throated Hummingbird (Archilochus colubris) tongue tip protruding from the bill tip. (C) Dorsal view of the morphology of a hummingbird tongue (approximate dimensions for A. colubris) showing length of the entire tongue, open-sided grooves, and the fringed (lamellar) region of the tip (distal approximately 6 mm). Base of the tongue is on the left; tip on the right. (D) Cross-sectioning shows the structural arrangement along the distal region of the tongue; green arrows identify the placement of the cross-sections. Black lines indicate the same structures in dorsal and cross-sectional views. Note the change in position of supporting rods from the base of the grooves to the tongue tip. Unlabeled scale bars, 0.5 mm.


https://www.youtube.com/watch?v=dMw3RO7p9yg



Fig. 2.
Hummingbird tongue trapping nectar. (A) Dorsal view of a post mortem tongue tip (A. colubris) leaving nectar, from totally immersed (Top photograph) at 0 milliseconds (ms), to outside the liquid (Bottom photograph). Green arrows mark the same reference point on the tongue in each image. (B) Cross-sectional diagrams (right margin) indicate the changes in position of lamellae at the reference point over time. From top to bottom: inside rotation of the entire structure (blue and red colors represent portions of visible lamellae along each side of the rod), tongue tips joining, and lamellae closing. In the first two diagrams, lamellae are inside the nectar; in the last two, lamellae have been withdrawn but contain nectar trapped inside the grooves. Scale bars, 0.5 mm.



Fig. 3.
Conceptual hypothesis of the forces involved in lamellar closing. Blue arrows indicate the force exerted by surface tension (γ). Black arrows represent the Laplace pressure (p). (A) Dorsal view of a post mortem tongue (A. colubris) interacting with the air–nectar interface, showing the change in lamellar position with respect to the change in meniscal width (sagittally inclined yellow arrows). (B) Cross-section diagrams indicating the surface energy gradient on the internal menisci outside the nectar (Left) and at the beginning of the interface (Right). Yellow arrows depict meniscal width matching the points in the Upper panel. (C) Conceptual representation of the main forces acting on each lamella. Note that the minimum surface area state is achieved outside the nectar (Left) and the maximum surface area state is reached at the beginning of the interface (Right). When the tongue is leaving the nectar and the fluid no longer covers the outer wall of the lamella, the external component of the surface tension (γe) stops operating on the structure, Laplace pressure (p) begins to act and the surface area tends to be reduced by the internal component of surface tension (γi). The net result is the bending of the flexible lamella over the stiffer rod. Scale bar, 0.5 mm.



Fig. 4.
Conceptual hypothesis for lamellar movements during the licking (tongue) cycle. (Left column) Frames from the high-speed videos showing a lateral view of the bill tip and the tongue of a living Indigo-capped Hummingbird (Amazilia cyanifrons). Green arrows identify the cross-sections denoted in the middle column. (Center column) Cross-sections of the tongue tip showing the shape of the lamellae on each frame in the Left column. (Right columns) Conceptual depiction of the hypothesized relative contributions of the most important contributors to lamellar movements on each shape of the lamellae. Red stands for elastic potential energy (Ue), blue for surface energy (γA), and black for Laplace pressure (p). (A) The cycle begins when the tongue is protruded through a narrow space left when the bill tips are separating from each other. (B) Tongue penetrating the nectar located in the artificial feeder on the Left. (C) Maximum protrusion distance of the tongue in this licking cycle. (D) Tongue leaving the fluid while being retracted inside the bill. (E) Tongue almost fully retracted inside the bill; when the bill closes the cycle starts again. Scale bars, 1 mm.


Hummingbird tongues are elastic micropumps 8
Pumping is a vital natural process, imitated by humans for thousands of years. We demonstrate that a hitherto undocumented mechanism of fluid transport pumps nectar onto the hummingbird tongue. Using high-speed cameras, we filmed the tongue–fluid interaction in 18 hummingbird species, from seven of the nine main hummingbird clades. During the offloading of the nectar inside the bill, hummingbirds compress their tongues upon extrusion; the compressed tongue remains flattened until it contacts the nectar. After contact with the nectar surface, the tongue reshapes filling entirely with nectar; we did not observe the formation of menisci required for the operation of capillarity during this process. We show that the tongue works as an elastic micropump; fluid at the tip is driven into the tongue's grooves by forces resulting from re-expansion of a collapsed section. This work falsifies the long-standing idea that capillarity is an important force filling hummingbird tongue grooves during nectar feeding. The expansive filling mechanism we report in this paper recruits elastic recovery properties of the groove walls to load nectar into the tongue an order of magnitude faster than capillarity could. Such fast filling allows hummingbirds to extract nectar at higher rates than predicted by capillarity-based foraging models, in agreement with their fast licking rates.


The hummingbird tongue fills with nectar even when only the tip is immersed. (a) Hummingbirds can drink from flowers with corollas longer than their bills by extending their bifurcated, longitudinally grooved tongues to reach the nectar. During protrusion, the tongue is compressed as it passes through the bill tip, which results in a collapsed configuration of the grooves (cross-section). (b) Upon reaching the nectar, the tongue tips fringed with lamellae roll open and spread apart, but some of the grooved portions of the tongue will never contact the nectar pool. For the grooves to fill with nectar, they must return to their uncompressed, cylindrical configuration. (c) Coronal cutaway from a µCT scan showing the bill and tongue architecture. Hummingbird drawn by K. Hurme.

The cylinders are in a flattened shape when they enter the nectar. Having been compressed by the beak, they store elastic energy that makes them rapidly expand in the fluid as they unfurl. This expansion helps to pump the fluid into the cylindrical cavity upward from the lamellae. That way, more nectar can be delivered into the bird’s mouth. 9

https://www.youtube.com/watch?v=QYoYQAbPXbU




Blue whale tongues weigh almost 6,000 pounds. That's as much as African forest elephants weigh! They probably use their giant tongues to pick some of the thousands of pounds of krill out of their toothbrush bristle-looking baleen plates.
Some snakes use folds of skin in their mouths to soak up water like a sponge through a mechanism called capillary action, a 2012 study found.
Pangolins, a relative of anteaters, have long, sticky tongues supplied by an overactive salivary gland that they use to eat thousands of ants. The mammals are hunted in parts of Asia for their meat and scales, and are critically endangered.
The okapi, which is related to giraffes and looks kind of like a zebra, has a tongue so long it can lick its own eyes and ears. The animal uses its lengthy tongue to strip leaves off of trees and into its mouth.
Dogs make little cups out of their tongues when they drink water, and they are much sloppier than cats.

https://www.youtube.com/watch?v=0hb7E7IjrFc


Cat tongues make cups, too. Felines create a column of water under their tongue when they elegantly place it on the surface of the liquid. Mesmerizing, isn't it?
Mallee fowl don’t sit on their eggs, like most birds do to let their body heat incubate the eggs. They build a large mound and monitor its temperature with their bill and tongue.  The hen usually begins laying in late September — the southern hemisphere spring. From that time until about April, the male uses his beak and tongue to ensure that the temperature of the mound stays constant.

1. http://www.dandydesigns.org/id54.html
2. https://hiddeninjesus.wordpress.com/2012/10/21/intelligent-design-woodpecker-tongue/
3. http://www.present-truth.org/3-Nature/Evolution%20of%20Creationist/MOGC%2010.htm
4. http://www.hiltonpond.org/thisweek030308.html
5. http://creationrevolution.com/scientists-discover-design-features-of-woodpecker-pecking/#f7tW1TdAfzoOuBTo.99
6. http://www.bbc.co.uk/news/science-environment-15458633
7. https://evolutionnews.org/2015/09/hummingbird_ton/
8. http://rspb.royalsocietypublishing.org/content/282/1813/20151014
9. https://evolutionnews.org/2015/09/hummingbird_ton/
10. https://books.google.com.br/books?id=URxlAgAAQBAJ&pg=PA22&lpg=PA22&dq=tongue,+intelligent+design&source=bl&ots=vlKC_TMAG-&sig=cYc-8Pt_3XUbOukq7sgSp-ua_eM&hl=pt-BR&sa=X&ved=0ahUKEwi-_pu9__bUAhVKfiYKHW8GAzMQ6AEIUzAH#v=onepage&q&f=true
11. http://www.businessinsider.com/craziest-ways-to-drink-in-the-animal-kingdom-2015-10/#dogs-make-little-cups-out-of-their-tongues-when-they-drink-water-and-they-are-much-sloppier-than-cats-11
12. http://www.brighthub.com/science/genetics/articles/45935.aspx
13. http://factslegend.org/20-interesting-human-tongue-facts/
14. https://www.newscientist.com/article/dn27181-tongues-may-have-evolved-from-a-mouthful-of-water/
15. https://academic.oup.com/molehr/article/19/6/349/1061673/Taste-perception-from-the-tongue-to-the-testis
16. http://www.nature.com.sci-hub.cc/nature/journal/v444/n7117/full/nature05401.html
17. http://bio1152.nicerweb.com/Locked/media/ch50/taste.html

More readings:
The Craziest Tongues In Nature
http://www.ranker.com/list/crazy-animal-tongues/eric-vega



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Tongue Erections Help Bats Sop Up Nectar 1





Bats use erectile tissue to drink. But don't worry — the tissue is on their tongues. Nectar-eating bats lap up the sweet liquid by engorging their tongues with blood, which, in turn, makes hairlike projections on the tongue stand at attention, new research finds. Together, the erect hairs, called papillae, act like a mop that grabs more liquid than a smooth surface could alone. Video of the process shows that as the bat reaches out to grab the nectar, its tongue turns bright red as blood automatically rushes in. 

Hairy tongues
Scientists have long known that nectar-feeding bats have hairy-looking tongues, as do hummingbirds and other species that rely on flowers for food. These hair projections are called papillae, which are specialized versions of the bumps that dot the tongues of humans and other mammals. Many human papillae host taste buds, but the hairlike papillae on bats show no signs of sensory tissues. (Bats’ taste buds are further back on their tongues.) Anatomists also have noticed large blood vessels in these bats' tongues, Harper told LiveScience. "I thought, 'Oh, that's really interesting that there are these enlarged blood vessels and these really specialized papillae,'" Harper said. "There's the possibility that maybe blood flow was used to move these papillae during feeding." Dissections of bat tongues revealed that there were sinuses, or spaces, along the sides of the tongues that extended into the papillae, suggesting blood flowed through the millimeter-long hairs. Harper and her colleagues just had to find out whether the papillae moved during feeding. To do so, they set up high-speed video cameras around feeding stations and let the nectar-eating bat Glossophaga soricina have at the sweet spots. Nectar-feeding bats have keen spatial memory and return to the same spots to feed again and again, Harper said. "All I had to do was make sure my feeder full of sugar water was set up in the same location, and then all I had to do was sit and wait," she said.

Mopping up nectar
At 500 frames per second, the videos showed that as the bats extended their tongues, at first, the papillae were flat against the tongue surface. But then, as the tongue hit its maximum elongation, the hairs became erect. Color video revealed that this change in position occurred as the tongue tip flushed bright red. "The hairs separate from each other, and that creates a little space between each of the rows of hairs on the tongue," Harper said. "Each one of those spaces becomes filled with nectar." The process is automatic, and likely driven by muscular tension in the tongue, Harper said. She and her colleagues report their findings today (May 6) in the journal Proceedings of the National Academy of Sciences. Mammalian penile erections also use blood to create stiffness, with arteries dilating to fill the penis with blood as contracting muscles prevent that blood from draining back to the body.
Bat tongues are just one of many animal features with promise for human engineering. Scientists have studied snail shells to develop stronger body armor, sticky gecko feet to inspire better adhesives, and insects to engineer miniature flying robots.

1. http://www.livescience.com/29346-tongue-erections-nectar-bats.html



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Science Advances: Deep-Dipping, Grooved Tongue Helps Bats Feast on Nectar 

Researchers have captured on video what appears to be a new tongue mechanism some bats use to feast on nectar. The researchappears in the 25 September issue of the journal Science Advances.
Nectar is a primary food source for many animals but a few, including hummingbirds, honey eaters and sun birds and bats, possess mouthparts specifically designed to slurp up the sweet liquid found in flowers. Specialized nectar-feeding bats typically siphon nectar from flowers using extremely long, protruding tongues sprinkled with hair-like papillae. But some bats sport another type of grooved tongue — one that scientists haven't studied in depth. 1

https://www.youtube.com/watch?v=1Wlxf2ttwe4


Marco Tschapka at the University of Ulm and colleagues show that grooved-tongued bats in the group of New World leaf-nosed bats known as the Lonchophyllinae display a unique feeding behavior. Using high-speed cameras focused on bats trained to obtain nectar from artificial "test tube" flowers containing honey water in the lab, the researchers' video captured bats hovering in short flights (rarely lasting a second) over the feeders.
Unlike bats with hairy papillae, which moved their tongues in short lapping movements resembling a cat, the grooved-tongued bats lowered their tongues into the test tubes and did not move them during the entire visit. The bats' grooved tongues appear to never separate from the liquid nectar, acting a bit like a conveyor belt to transport the food up the tongue and straight into the animals' mouths.
The researchers aren't exactly sure how the bats are able to do this, but suspect it occurs by some combination of tongue deformation and the ability of fluids like nectar to flow without external force in certain narrow spaces, a phenomenon known as capillary action.



THE GROOVE-TONGUED LONCHOPHYLLA ROBUSTA BAT VISITS A BROMELIAD FLOWER. | M. TSCHAPKA/ UNIVERSITY OF ULM


Both methods for obtaining nectar were effective, but the researchers think that the grooved-tongue bats may have an advantage in acquiring nectar from flowers of certain shapes that hold the sweet liquid differently.
For example, some flowers have diffusely distributed nectar, while others offer one small pool of nectar. Different nectar extraction mechanisms might be useful depending on the flower. The pumping mechanism of Lonchophyllinae bats might work more efficiently in flowers that allow a more complete submersion of the tongue in the nectar pool, the authors suggest.
Another important factor might be nectar viscosity. Nectar from bat-visited flowers is generally dilute, but the sugar concentration in nectar varies between flowers. Nectar with a low sugar concentration that is less viscous and more free-flowing might be more easily harvested by the pumping mechanism compared to nectar of high sugar concentration and viscosity.
Nectar uptake in bats using a pumping-tongue mechanism  2

Abstract

Many insects use nectar as their principal diet and have mouthparts specialized in nectarivory, whereas most nectar-feeding vertebrates are opportunistic users of floral resources and only a few species show distinct morphological specializations. Specialized nectar-feeding bats extract nectar from flowers using elongated tongues that correspond to two vastly different morphologies: Most species have tongues with hair-like papillae, whereas one group has almost hairless tongues that show distinct lateral grooves. Recent molecular data indicate a convergent evolution of groove- and hair-tongued bat clades into the nectar-feeding niche. Using high-speed video recordings on experimental feeders, we show distinctly divergent nectar-feeding behavior in clades. Grooved tongues are held in contact with nectar for the entire duration of visit as nectar is pumped into the mouths of hovering bats, whereas hairy tongues are used in conventional sinusoidal lapping movements. Bats with grooved tongues use a specific fluid uptake mechanism not known from any other mammal. Nectar rises in semiopen lateral grooves, probably driven by a combination of tongue deformation and capillary action. Extraction efficiency declined for both tongue types with a similar slope toward deeper nectar levels. Our results highlight a novel drinking mechanism in mammals and raise further questions on fluid mechanics and ecological niche partitioning.

INTRODUCTION

Nectar is an easily attainable resource because it is openly provided and advertised by flowers in return for pollination services from floral visitors. Its predominant components are various sugars that are used by the visitors as an energy source (12). Nectar is therefore a highly sought-after food item, primarily by invertebrates, but is also regularly consumed by vertebrates, including a few reptiles, birds, and mammals (34). Nectarivorous insects regularly consume floral nectar as their principal diet, whereas most nectar-feeding vertebrates are opportunistic users of floral resources. Accordingly and in contrast to many insects that have mouthparts specialized in nectarivory, very few obligate nectar-feeding birds (hummingbirds, honey eaters, and sunbirds) and mammals (the honey possum Tarsipes rostratus and various species of bats) show corresponding morphological specializations, mainly of the tongue (45).
Nectar-feeding bats constitute the largest number of specialized nectarivorous mammals and are found in two families: the Old World fruit bats (Pteropodidae) and the New World leaf-nosed bats (Phyllostomidae) in a number of genera traditionally placed in the subfamily Glossophaginae (67). Floral nectar is generally extracted from flowers by protrusible tongues that may even exceed the body length of bats and are covered with long hair-like papillae (89). However, some nectar-feeding bat genera present a strikingly different tongue morphology. Here, elongated papillae are almost absent, whereas deep longitudinal grooves run laterally along the entire length of the tongue (fig. S1). On the basis of these “markedly different adaptations for nectarivory,” Griffiths (10) first proposed a taxonomic separation of these species but offered no explanation as to the function of these morphological structures. After some debate on the validity of this proposal (1113), the recent molecular consensus is that groove-tongued bats form the subfamily Lonchophyllinae, which is a sister group to several predominantly frugivorous subfamilies, and that the subfamily Glossophaginae sensu strictu is the sister group to all of these subfamilies (1415). Considering these phylogenetic relations and the divergent lingual morphology (tongues with hair-like papillae versus grooves), we hypothesized that independently evolved nectarivorous habits should result in distinct differences in nectar-feeding behavior between the two taxa. We predicted that the differences in tongue morphology between glossophagine and lonchophylline bats would translate into drastic differences in tongue movement patterns. Behavioral differences could in turn lead to different nectar uptake and extraction efficiency in the two groups of nectar-feeding phyllostomids. Using a high-speed camera, we compared nectar uptake behavior between species representing both clades (the groove-tongued Lonchophylla robusta and Glossophaga soricina, which show a tongue with hair-like papillae) and measured extraction efficiency at different nectar levels.

Tongue movements

All bats visited the feeders in short hovering flights rarely lasting longer than a second. High-speed video recordings revealed distinct differences in tongue movement patterns between the two species. Upon inserting its snout into the feeder opening, G. soricina initiated repeated sinusoidal movements of the tongue, which alternated between dipping into the nectar and retracting into the mouth (Fig. 1A and video S1). The amplitude of tongue-tip movements was ca. 25 mm at a distance of 20 mm between the fluid level and the rim of the feeder. These discrete lapping movements were rather stereotypic and were repeated four to seven times per visit.



Fig. 1Tongue movement.
(Left) Extended tongues of drinking: (top) G. soricina (Glossophaginae) and (bottom) L. robusta (Lonchophyllinae). Although the tongue of G. soricina is covered by long filiform papillae, the tongue of L. robusta shows a distinct lateral canal. (Right) Movement patterns of the tongue tips of G. soricina (A) and L. robusta (B) drinking at a feeder offering honey water at 20 mm below the opening. The tongue of L. robusta submerges in the fluid at the beginning of the visit and stays there with only small movements, whereas the tongue of G. soricina extends and retracts repeatedly in stereotypic lapping movements. Interruptions of Glossophaga curves near the upper rim of the feeder represent the total retraction of the tongue into the mouth. (Left, center) Phylogenetic relations between the two groups [modified from (14, 27)] (figs. S1 and S2 and videos S1 to S4).

In contrast, L. robusta lowered its tongue into the fluid at the beginning of a feeding visit and maintained this position during the entire visit without any intermittent retraction into the mouth (Fig. 1B and video S2). The amplitude of the tongue tip was generally small (<5 mm) and was also partly related to the movements of the bat hovering above the feeder. Close-up recordings with the high-speed camera showed that the tongue tip assumed an almost horizontal position just below the nectar surface, with lateral grooves widely open. Although frontal views showed no distinct tongue deformation during drinking, lateral recordings showed peristaltic movements along the edges of the groove and fluid moving along the canal (video S3). The edges of the canal (up to 2 mm deep) are unconnected over the entire length of the tongue and therefore do not form a hermetically closed tube. However, we suggest that muscular action largely closes the edges, supported by a row of elongated triangular papillae that spring from the ventral edge and loosely cover the canal (fig. S2). Feeding was possible once the very tip of the tongue had been submerged in the nectar (video S4). Although the edges of the canal (in proximity to the bat’s mouth) remained in tight contact with each other, it was possible to see fluid rising up into the mouth shortly after the initiation of drinking.
In a quantitative comparison (see Statistical Analysis of Tongue Movement), the species showed significant differences in tongue movement patterns (Mann-Whitney U test: Z = −2.121,N1 = 4, N2 = 3, P = 0.034). Correspondingly, G. soricina individuals retracted their tongues significantly more often than did L. robusta individuals [Mann-Whitney U test: Z = −2.223, N1 = 4, N2 = 3, P = 0.026; median, 6.5 (G. soricina) and 1 (L. robusta)].

Nectar extraction efficiency

Artificial flowers were presented on a precision balance and the amount of nectar extracted after each visit was recorded. Visit duration was timed using light traps connected to a computer. Nectar extraction efficiency was defined as grams of nectar per second of hovering and was standardized on the basis of daily energy expenditure to account for differences in body size. We recorded 354 visits from 8 G. soricina individuals at nectar levels from 10 to 40 mm and 516 visits from 10 L. robusta at nectar levels between 10 and 50 mm.
At all nectar levels, the larger L. robusta individuals extracted more nectar than did the small G. soricina individuals (mean ± SE; L. robusta: 0.11 ± 0.01 g; G. soricina: 0.06 ± 0.01 g). Uptake steadily decreased in both species when bats had to extend the tongue farther down to lower nectar levels into the feeder (Fig. 2A). Both species showed a tendency to hover and feed longer at decreasing nectar levels (Fig. 2B). However, upon reaching the limit of their tongue extension capability, the bats tended to abort an unproductive feeding attempt, and hovering duration decreased. The standardized extraction efficiency declined significantly with decreasing nectar levels [general linear mixed modeling (GLMM); F4,75.014 = 50.009, P < 0.0001, Akaike information criterion = −676.452]. Even after correction for size difference, L. robusta was significantly more efficient than G. soricina (GLMM; F1,77.216 = 41.395, P < 0.0001); however, the observed decline in efficiency toward deeper nectar levels progressed similarly in both species (linear regression; L. robustay = 0.006 − 0.001xG. soricinay = 0.005 − 0.001x) (Fig. 2C). The interaction between nectar level and species had no significant influence on extraction efficiency (GLMM; F3,74.632 = 1.264, P = 0.293).





Fig. 2 Feeding behavior.
(A) The amount of nectar extracted after each visit decreases steadily toward deeper levels. (B) Hovering duration in G. soricina and L. robusta increases when bats have to reach deeper into the feeder. The final decline occurs when bats abort their visit upon reaching the limit of their tongue extension capability. (C) Standardized extraction efficiency in both species decreases at a very similar slope. All figures are presented as mean ±1 SE. (D) L. robustavisiting a bromeliad flower (Werauhia sp.). Photo was taken at the Bocas del Toro Field Station of the Smithsonian Tropical Research Institute on March 2009.

DISCUSSION

Animals extract nectar from flowers principally using one of three mechanisms: active suction, capillary suction, and viscous dipping (16). The drinking behavior of G. soricina has been investigated previously and consists of stereotypic lapping movements of an elongated tongue, assisted by long papillae (17) that are hemodynamically actively erected and help in effectively mopping up nectar out of a flower (18). This behavior has been classified as viscous dipping, and variations have been found in ants and bees (16). In contrast, the specific and so far undescribed nectar uptake technique of L. robusta transports nectar in deep lateral canals inside the tongue (fig. S1) (10). No lapping movements are observed. Instead, the tongue tip enters the fluid and remains submerged during the entire visit, and nectar is actively pumped into the bat’s mouth. All nectar-feeding mammals studied so far use variations of the brush-tongue lapping technique, whereas grooved tongues seem to be specific for Lonchophylla and some closely related genera (Lionycteris, Platalina, Xeronycteris, and Hsunycteris). Future investigations will probably reveal that all species in this clade share the use of a pumping-tongue drinking mechanism. The pumping tongue’s highly dynamic lingual canal system is not tightly sealed when active, which becomes obvious when the fluid rises and the opening of the canal becomes visibly moist. Feeding through active suction along the entire length of the canal (as found, for example, in moths and butterflies) (16) is therefore not possible because the semiopen canal cannot support the buildup of a necessary pressure difference. Nectar is probably extracted through a combination of active pumping movements of the canals realized through complex bundles of skeletal muscles (10) and capillary forces in small canals. By loosely connecting both sides of the tongue canal, triangular papillae (fig. S2) might additionally help to minimize leakage. As in G. soricina and other glossophagine species (19), the amount of food extracted by L. robusta decreased with lower nectar levels, which was partly compensated for by an increased duration of foraging. Given the fundamental differences between nectar uptake mechanisms, it is remarkable that standardized feeding efficiency decreased in both species at almost the same rate because they could be affected by different parameters. Loss of efficiency in brush-tongued bats at deeper flowers might be mainly attributable to shorter tongue-nectar contact per licking cycle and leakage during tongue retraction. In contrast, the complex muscular arrangement of a grooved tongue at near-maximum extension might progressively lose its degree of mobility, resulting in a decrease in pumping efficiency.
The drastic differences in nectar extraction techniques between L. robusta and G. soricina are striking given their rather close phylogenetic relationship. Apparently, nectarivory has independently evolved twice in a relatively small group of bat species, realizing two totally different methods that functionally only share the enormous elongation of the tongue in common. Because bat-pollinated flowers seem to be at least basically accessible to both convergently developed nectar extraction mechanisms, selection from one bat clade might have indirectly increased the number of floral partners and resource availability in the other clade, thus initially stabilizing the dichotomy.
Species from both clades co-occur in most regions of the neotropics from southern Mexico to Peru, Bolivia, and Brazil (20, 21). This coexistence suggests that nature offers fitting niche options for both. The nectar volume of bat-pollinated flowers ranges from less than 0.05 ml to more than 10 ml in one night (22–24). Some flowers have diffusely distributed nectar, whereas others present one small pool of nectar. The different nectar extraction mechanisms of the two nectar-feeding bat clades might correlate with this variability in nectar volume and distribution in flowers. It is feasible that small and distributed nectar quantities are more efficiently mopped up by the long hair-like papillae of the glossophagine tongue. In contrast, the pumping mechanism of Lonchophyllinae could work more efficiently in flowers that allow a more complete submersion of the tongue in the nectar pool. In fact, the significantly higher standardized extraction efficiency observed in Lonchophylla could be partly attributable to our experimental setup, with copiously available nectar that might have favored the pumping mechanism. Another important parameter, which is hardly studied in bat flowers, might be nectar viscosity. Nectar from bat-visited flowers is generally rather dilute, but sugar concentrations range between 4% and nearly 30% (23). Although this is far from the extremes found in nature, nectar of low sugar concentration and viscosity might be more easily harvested by the pumping mechanism than nectar of high sugar concentration and viscosity (16). The different extraction mechanisms described here might match the nectar presentation of some flowers better than others and thus could ultimately provide possibilities for resource partitioning and coexistence of species (Fig. 2D).
In conclusion, our study reveals a specific and hitherto undescribed nectar pumping system in lonchophylline bats that represents a convergent evolution to the brush-tip tongues of glossophagine bats and provides similar feeding efficiency. This new mammalian drinking mechanism raises both mechanistic and ecological questions. For a full functional understanding of the pumping mechanism, it will be necessary to study fluid dynamics and the interaction between active tongue movements and passive capillary actions. In an evolutionary and ecological context, it might be rewarding to evaluate the nectar presentation patterns of chiropterophilous flowers for suitability for the two different methods of nectar extraction.

MATERIAL AND METHODS


Experimental design for tongue movement

Using high-speed video recordings, we compared the nectar-drinking behavior of the Pallas’ long-tongued bat G. soricina (the most common glossophagine species with a brush-tip tongue) to that of the orange nectar-feeding bat L. robusta (a lonchophylline species with a grooved tongue). Experiments with G. soricina were performed in an experimental chamber (4.8 m by 2.4 m by 2.2 m) between September 2009 and August 2010 using bats from a captive colony at the University of Ulm (Ulm, Germany). L. robusta bats captured temporarily from the wild were tested in a flight tent (4 m by 4 m by 2.5 m) at the Bocas del Toro Field Station of the Smithsonian Tropical Research Institute (Balboa, Panama) in March 2009.
Bats (L. robusta, n = 3; G. soricina, n = 4) were recorded visiting a glass tube (10.3 mm by 5.5 mm by 100 mm) filled with artificial nectar (honey water, 17% w/w sugar concentration) up to 20 mm below the opening. All video recordings were made under infrared light-emitting diode light (Sony HVL-IRM) using a black-and-white high-speed camera (Optronis Camrecord 600x2) with Nikkor 60- or 100-mm macro lenses (Nikon) set to 500 to 750 frames/s for 1/1000 to 1/3003 s of exposure. Tongue-tip insertion into the feeder was tracked on all available video frames using ImageJ software (25).

Statistical analysis of tongue movement

We analyzed tongue movements after full extension during the initial insertion at successive 75-ms intervals, which approximately corresponded to the duration of tongue extraction and retraction of lapping G. soricina. We calculated the slope for each interval using linear regressions and averaged absolute slope values for each individual as a proxy for tongue movement patterns. Subsequently, we performed a Mann-Whitney U test on mean slope values to determine species-specific differences in tongue movements. We additionally counted the number of tongue retractions after the initial insertion for all seven individuals and conducted a Mann-Whitney U test to investigate species-specific differences.

Experimental design for nectar extraction efficiency

G. soricina (8 individuals; mean ± SD body mass, 10.7 ± 0.6 g) and L. robusta (10 individuals; mean ± SD body mass, 15.4 ± 1.7 g) visited test tubes (9 mm in diameter) placed on an analytical balance (precision, 1 mg; Mettler Labstyle 152) and filled with nectar at different distances from the upper rim (10, 20, 30, 40, and 50 mm). Readings before and after a visit provided the mass of consumed nectar. An infrared light beam at the entrance of the test tube allowed us to register bat visits on a personal computer (precision, 10 ms) using a custom-written program (Turbo Pascal 5.0). Time differences between subsequent light beam status changes provided the duration of each hovering visit. We defined nectar extraction efficiency, E(g/s), as the ratio of the benefit of a flower visit to the cost of a flower visit [that is, extracted honey water (g) and hovering duration (s)] following an established protocol (19).

Statistical analysis of nectar extraction efficiency

For a biologically meaningful comparison among differently sized species, we standardized the nectar extraction efficiency Es by dividing E by the species-specific daily energy expenditure DEE, which is a function of body mass (1926). We used GLMM (normal distribution, identity link function) to compare the standardized nectar extraction efficiency in both species. Fixed effects included species, honey water level, and species–honey water level; individual bats were included as random effect. All calculations were run in Excel 2007 (Microsoft Corp.). Statistical tests were performed with SPSS version 20.0 (IBM).

1) http://www.aaas.org/news/science-advances-deep-dipping-grooved-tongue-helps-bats-feast-nectar
2) http://advances.sciencemag.org/content/1/8/e1500525.full



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4 Chameleon Tongues on Fri Jul 07, 2017 1:52 pm

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Chameleon Tongues

The chameleon also has one of the fastest tongues on the planet.  It is so fast, in fact, that it is difficult for the human eye to see it when the lizard shoots it at potential prey (which may be more than a body length away). Just how fast is this super-hero-like tongue? Scientists have discovered that the chameleon’s tongue can accelerate five times faster than a fighter jet. Now that is fast!

The design we see in nature is powerful evidence for the existence of God. Indeed, it is so powerful that it forced world-renowned atheist Antony Flew to admit his lifetime of scholarship was wrong and that God must exist. The more we learn about this planet and the life on it, the more we stand in awe of that amazing design. The chameleon is an excellent example of this trend. For a long time, scientists have known about the amazing design features of the chameleon. The more we learn, however, the more amazing chameleons become! 1

Terrific tongue 2
The chameleon needs this fine judgment of distance to capture prey with its tongue. This is another remarkable feature—the tongue can reach up to 1½ times the lizard’s body length. The acceleration of this ‘ballistic tongue’ is amazing—50 g (i.e. 50 times the acceleration due to gravity), while astronauts and jet fighter pilots will pass out at only 10 g. The chameleon uses special supercontracting muscle, ‘unique among vertebrates’ and otherwise found only in invertebrates. This is necessary to produce the tension over the great changes in muscle length. A special high-speed X-ray camera is required for scientists to film the tongue through its entire movement (including inside the mouth)

For quite some time, biologists have puzzled over why a chameleon’s tongue is not affected by the temperature. After all, chameleons are cold-blooded. In other words, they cannot regulate their internal body temperature. As a result, their internal body temperature changes with the temperature of their surroundings. The colder the surroundings get, the colder the internal temperature of a chameleon gets.

Well, the colder the temperature, the slower the chemical reactions that power an animal’s muscles. Because of this, cold-blooded animals show a significant reduction in muscle action the colder the surroundings become. However, a chameleon’s tongue shows no significant reduction in action, even when the temperature dips almost to the freezing point of water! This is strange, because the tongue is a muscle, and all the chameleon’s other muscles are affected by temperature. Why not the tongue? Biologists now know the answer to that question, and it is remarkable.



When the chameleon wants to shoot its tongue out of its mouth to nab its prey, it doesn’t rely as much on its muscles. Instead, it relies on all that stored energy in the elastic collagen that is in its tongue. So the elastic collagen stores up a lot of energy as it is being compressed, and then when it is released, the energy stretches out the collagen, and the tongue along with it. As the author of the Science News article states:

Using elastic collagen instead of muscle power to shoot its tongue at prey lets a chameleon catch breakfast even when its muscles are stiff from the cold…

Of course, this is just what you would expect from a Master Designer. God knows that the chameleon needs a fast tongue to catch its prey. It doesn’t need to retract its tongue quickly. After all, once the prey is caught, a few more seconds to “reel it in” won’t matter. However, even a fraction of a second too slow when it comes to shooting out its tongue, and the prey is never caught. As a result, God designed a system that allows the muscles to work on retraction, but not so much when it comes to shooting the tongue out of the mouth. We live in an amazingly engineered world! 3

https://www.youtube.com/watch?v=E76YBF3P0K0


Chameleon has one of fastest tongues in animal kingdom 4
Chameleons’ long, elastic tongues are one of the fastest muscles in the animal kingdom, extending more than twice their body length and packing 14,000 watts of power per kilo. But it is the smallest species that strike fastest, according to a new study. Researchers filmed tongue strikes of chameleons attacking a suspended cricket, at 3000 frames per second. They found that the animals’ tongues are capable of impressive acceleration, doing 0 kilometers to 100 kilometers per hour in one-hundredth of a second, twice as fast as the fastest car. And, like sports cars, the smallest chameleons are the most powerful. Across 20 species, ranging from the tiny 1-cm rosette-nosed chameleon (Rhampholeon spinosus) to the half-meter Malagasy giant chameleon (Furcifer oustaleti), the team found that smaller species’ tongues could accelerate at more than 250 g, five times faster than that of the largest chameleon. This is because small chameleons have evolved larger tongues relative to their body size, handy since they also need to consume proportionally more food to survive. As well as raw muscle power, chameleons spring-load the elastic tissue in their tongue, catapulting it toward prey when they strike, and giving them the highest acceleration and power output of any reptile, bird, or mammal. Previous studies underestimated their power because they failed to consider the little guy.

https://www.youtube.com/watch?v=dm1iHi-38kk


In contrast to the limb muscles, the tongue muscles of chameleons are anything but slow; they produce high forces for their cross-sectional area. These unusually fast, ballistic tongues permit them to capture a
wide variety of prey. The super contractile tongue-retractor muscles are unique among vertebrates and allow them to reel in even large vertebrate prey. 5

The South African chameleon species Bradypodion thamnobates releases its tongue with up to 41,000 watts of power per kilogram of muscle involved. Previous studies didn’t record anything so high because they focused on larger chameleons, the Brown University study said. When comparing body-size relationship with tongue performance, smaller species had tongues that were much more powerful that bigger ones in various mouth athletics. 6

Manipulators inspired by the tongue of the chameleon 10

Chameleons have developed a specialized ballistic tongue which elongates more than six times its rest length at speeds higher than 3.5 m s−1 and accelerations 350 m s−2, with a highly flexible mobile part, and which applies no continuous force during forward motion. These characteristics are possible because this tongue consists of two highly specialized systems, an ejection system for the forward motion and an accordion-like system for the retraction.

Had the two systems not have to emerge TOGETHER? 

The chameleon is a lizard, which appeared 120 million years ago. It evolved from the lepidosauria, also the ancestor of the snake, the skink, and the gecko, and developed many
specializations not found in other reptiles (Vitt et al 2003). 10,11



Nowhere near we see that chameleons had a common ancestor with squids and frogs, which have the same features and ballistic tongue. Of course one can argue about converget evolution, but thats not supported by evidence. Its an unsupported claim. Convergence can also be explained by common design.



The tongue of the chameleon is part of a larger system called the hyolingual apparatus comprising the tongue, the hyoid, the hyoglossus complex, and the extralingual muscles. The terms lingual, glossal, and glossus refer to the
tongue. Figure 2(a) shows a simplified schematic view of the hyolingual apparatus of the chameleon. Except for the ceratobranchial, the drawing shows a cross-section of the system. The tongue, supported by a central bone called
the entoglossal process, contains two main parts. The first part, containing the accelerator muscle and the collagenous intralingual sheaths, cover the entoglossal process and is responsible for the projection of the tongue. The second part, situated at the tip of the tongue and called the tongue pad, contains several muscles, which actuate a deformable pocket, and is responsible for the catching of the prey. The entoglossal process connects to the head of the chameleon via two rods called the ceratobranchial. The hyoglossus complex is a long accordion-like complex which connects the accelerator muscle and the top of the ceratobranchial. It contains the hyoglossus muscle and the lingual nerve, and is responsible for the retraction of the tongue. The anatomy of the hyolingual apparatus of the chameleon is much more complex. The tongue is activated by 15 to 19 muscles or pairs of muscles depending on the species. Nerves, taste buds, and saliva glands are also present. Besides catching of prey by ballistic projection, the tongue is also used for prey processing, drinking, and grasping of fruits (Takahashi 2008).

This seems to me to be a extremely complex system that cannot be reduced , since several parts and mechanisms are essential to constitute a functional whole.

Salamander Tongue Is World's Most Explosive Muscle 7

The greatest burst of power from any animal muscle comes from the tongue of a tropical salamander, scientists have announced. The giant palm salamander of Central America (Bolitoglossa dofleini) captures fast-moving bugs with an explosive tongue thrust that releases over 18,000 watts of power per kilogram of muscle. 8 The salamander's ballistic firing permits the tongue's sticky-padded tip to reach prey in just a few thousandths of a second. Deban noted that the greatest power output from muscle acting alone has been measured in quail as they flap their wings in vertical takeoff.

"The salamander muscle produces 16 times the peak instantaneous power output of the quail, albeit by using the trick of elastic storage," Deban said, referring to the mechanism that fires the salamander's muscular "bow."

https://www.youtube.com/watch?v=zcWxAfl0okE&t=70s


https://www.youtube.com/watch?v=VzOGqNquM7Q


https://www.youtube.com/watch?v=teJu6lNuZxs


Salamander with a ballistic tongue 12
Lungless salamanders of the family Plethodontidae capture prey using the most enhanced tongue-protrusion mechanisms found in amphibians. Salamanders of the genus Hydromantes are the most extreme specialists, possessing tongues that can be shot with great accuracy at prey several centimeters away, reaching the target in a few milliseconds. We have found that the tongue of Hydromantes is a true projectile. It is fired from the mouth by a ballistic mechanism and is not simply an extrapolation of the general tongue-protrusion mechanism. The tongue reaches the prey under its own momentum.  Like all terrestrial salamanders, Hydromantes captures prey on a sticky tongue pad at the anterior tip of a folding tongue, supported by a skeleton of flexible, interlinked cartilages. This skeleton is part of the hyobranchial apparatus, a derivative of the visceral skeleton or gill arches of ancestral
vertebrates. The tongue skeleton is driven forwards by protractor muscles acting on its posterior ends and folds to the midline as it slides forwards.



Cuttlefish tongue, convergence with chameleons

https://www.youtube.com/watch?v=_atQW9b6qR8


Watch: A frog’s tongue is an ultrasoft shock absorber 9

https://www.youtube.com/watch?v=SfQlKAeiUNk


The sticky, elastic tongues of amphibians have fascinated researchers for decades—the first study of frog and toad tongues was done in 1849. However, the underlying physics of this adhesive feat remained unclear. Previous studies compared frog tongues to scotch tape, but that’s not the full picture, researchers report today in the Journal of the Royal Society Interface. Yes, frog tongues are uniquely sticky (and their saliva makeup is crucial in bug capture), but they’re also very soft—10 times softer than human tongues and one of the softest known biological materials. That softness makes frog tongues more like adhesive shock absorbers than scotch tape, the researchers suggest. Here’s what happens: Say a bug is buzzing by and a frog releases its tongue. When the bug hits the frog’s tongue, the tongue wraps around the bug like a sticky bubble gum blanket and absorbs the bug’s inertia. Upon impact, the bug gets coated in saliva. Because the tongue is so soft, it can stretch out more than twice its thickness to cover more of the bug’s surface area and get its saliva into the grooves of a bug’s bumpy exoskeleton. Frog saliva is a non-Newtonian fluid, the team found, meaning it defies Newton’s law of viscosity and its flow changes under stress. So the saliva flows normally until the bug hits it, and then the saliva grips the bug as the tongue is retracted back into the frog’s mouth. But if a frog’s tongue is so sticky, how does it get its meal off its tongue and into its stomach? In a much studied phenomenon, frogs swallow with their eyes. The researchers found that when the eyes push against the bug in a motion parallel to the tongue, the saliva starts to flow easily again and down goes dinner. And although the researchers no longer think frog tongues are all that similar to scotch tape, this new finding might help them design new adhesives that stick at high speeds.

1. http://blog.drwile.com/cameleon-tongues-another-example-of-amazing-design/
2. http://creation.com/a-coat-of-many-colours-captivating-chameleons
3. http://apologeticspress.org/DiscoveryPubPage.aspx?pub=2&issue=1168
4. http://www.sciencemag.org/news/2016/01/video-chameleon-has-one-fastest-tongues-animal-kingdom?utm_source=general_public&utm_medium=youtube&utm_campaign=chameleon-video-1702
5. The biology of Chameleons, page 33
6. http://www.dailymail.co.uk/sciencetech/article-3013546/The-amazing-gross-acrobatics-chameleon-tongue-revealed-slow-motion.html
7. http://news.nationalgeographic.com/news/2007/03/070309-salamander.html
8. http://news.nationalgeographic.com/news/2007/03/070309-salamander.html
9. http://www.sciencemag.org/news/2017/01/watch-frog-s-tongue-ultrasoft-shock-absorber
10. http://iopscience.iop.org.sci-hub.cc/article/10.1088/1748-3182/6/2/026002
11. http://aerg.canberra.edu.au/library/sex_general/2003_Vitt_etal_history_and_global_squamate_ecology.pdf
12. http://www.nature.com.sci-hub.cc/nature/journal/v389/n6646/full/389027b0.html


Further readings:
Chameleon Tongue Inspires Robotic Design
http://www.icr.org/article/chameleon-tongue-inspires-robotic-design/

Activation patterns of the tongue-projector muscle during feeding in the imperial cave salamander Hydromantes imperialis
http://jeb.biologists.org/content/207/12/2071?ijkey=c7992d1d40582fb4d966098f3b7dd19910ddefcf&keytype2=tf_ipsecsha

Evolution of the structure and function of the vertebrate tongue
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570891/

Secret of the chameleon's ballistic tongue revealed
http://www.dailymail.co.uk/sciencetech/article-3548250/Secret-chameleon-s-ballistic-tongue-revealed-Reptile-s-firing-mechanism-uses-three-parts-hit-fast-moving-targets.html



Last edited by Admin on Fri Jul 07, 2017 8:00 pm; edited 7 times in total

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5 Flamingo Tongues Are Weirdly Phallic on Fri Jul 07, 2017 3:30 pm

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Flamingo Tongues Are Weirdly Phallic 1

There are a couple things that make flamingo tongues way weirder than average. First are the spiny bristles that coat their tongues, an adaptation that allows them to filter their food much like baleen whales do. On top of these unusual spines, scientists have discovered erectile tissue. These are a crucial part in how flamingo tongues work. When feeding, this tissue will fill with blood and become rigid. Since flamingos feed by dipping their heads upside down in water, researchers hypothesize this swollen tissue assists in the stabilization of their heads. 1

Another study, published in Anatomical Record in 2006 by biologist Casey Holliday and professor of anatomy Lawrence Witmer from Ohio University, found erectile tissue in the flamingo’s beak. Flamingos are known for their odd way of eating – they stand in shallow water, and put their beaks in an almost upside-down position in the water to catch food as it floats by. Their tongues act like pumps that manipulate the water, squeeze the food out and trap it. When Holliday and Witmer constructed a 3D model of a flamingo’s head, they noticed large, oval-shaped masses of erectile tissue on the floor of its mouth and running along either side of its tongue. Just like the erectile tissue in a man’s penis, this stiffens when filled with blood – like when the head is tipped upside-down – and helps to strengthen and support the floor of the mouth and tongue when the flamingo is feeding. “We suspect this stabilises the mouth and tongue and helps with the peculiar way that flamingos eat,” said Witmer. “It’s an important new piece of the puzzle of flamingo feeding – frankly, a piece we hadn’t known was missing.” 2

1. http://www.ranker.com/list/crazy-animal-tongues/eric-vega
2. https://blogs.scientificamerican.com/running-ponies/flamingo-hows-wheres-and-whys-pink-errectile-tissue-one-leg/

More readings:
http://www.ohio.edu/people/witmerl/Downloads/2006_Holliday_Ridgely_Balanoff_Witmer_flamingo.pdf

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6 Chemosensory transduction on Sat Jul 08, 2017 7:36 am

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What emerged first, the taste buds, or the brain cortex that interprets the information, or the nerve that sends the signal from the taste buds to the brain ? what function does each of the 3 parts have without the other ?

Chemosensory transduction 1
Taste buds are sensory end organs that are located in the oral epithelium



The receptors on the chemosensitive apical tips of taste bud cells confer specificity to gustatory stimuli. Taste receptors come in many types, including several classes of G protein-coupled receptors (GPCRs) and ion channels (FIG. 1).




Some stimuli interact with receptors to generate second messengers, whereas in other instances, the taste stimulus itself is transported into the cytoplasm of taste bud cells and activates downstream events. Taste bud cells can be organized into three main types, in part according to their function. In general, bitter, sweet and umami stimuli are detected by type II cells1–3, sour stimuli are detected by type III cells4–6, and salty (NaCl) stimuli are detected by as-yet-undefined taste bud cells. Below, we describe the mechanisms by which gustatory stimuli are transduced by taste buds. Sweet and bitter are sensory perceptions; the compounds that elicit them are labelled with these
same names as a shorthand.

Sweet
Taste buds detect sugars (probably as an indication of carbohydrates) and other sweet stimuli using diverse mechanisms. The best-studied receptor for sweet stimuli is the heterodimer formed of two GPCRs: namely, taste receptor type 1 member 2 (T1R2) and T1R3. These subunits were identified by screening for mRNAs that are preferentially expressed in mouse taste buds8 or by genetic linkage to Sac, which is a locus known to dictate sweet-taste sensitivity in mice. When cultured cells are co‑transfected with T1R2 and T1R3, they respond to sucrose, fructose, artificial sweeteners and some d‑amino acids that elicit a sweet taste. T1R2 and T1R3 belong to family C of the G protein-coupled receptors (GPCRs) They each possess a long extracellular amino terminus that forms a venus flytrap module (VFM). T1R2 and T1R3 function as a heterodimer, and have multiple ligand-binding sites. Nevertheless, the purified extracellular domain alone of either T1R2 or T1R3 is capable of binding many sugars and sugar alcohols. Modelling and experiments with chimeric and point-mutated T1R2 and T1R3 have demonstrated that sugars and dipeptide sweeteners (for example, aspartame) bind in the cleft of the VFM, albeit at slightly different positions. Intensely sweet proteins (for example, monellin and brazzein) bind in the VFM and in a cysteine-rich domain that links the VFM to the transmembrane region, and small-molecule sweeteners (for example, cyclamate) bind at residues in or near the transmembrane domains. Mice that lack T1R2 or T1R3 have been reported to lose all behavioral sensitivity and neural responses to sugars and artificial sweeteners. However, another group has reported that knocking out the gene that encodes T1R3 (Tas1r3) variably affects responses to sugars while eliminating the detection of artificial sweeteners. This finding suggests that T1R3‑independent mechanisms probably exist for the detection of sugars and other sweeteners. One postulated T1R3‑independent mechanism involves glucose transporter type 4 (GLUT4) and sodium/glucose cotransporter 1 (SGLT1), which have been shown to transport glucose into sweet-sensing taste cells, leading to a transient elevation of intracellular ATP. ATP that is generated by this pathway blocks ATP-inhibited K+ channels (KATP channels) to depolarize the membrane. Disaccharides such as sucrose are hydrolysed to hexoses and can then activate this pathway. The involvement of a Na+-dependent transporter — that is, SGLT1 — in transducing sugars offers a plausible explanation for the potentiation of sweet taste by Na+ salts. T1R3‑independent pathways for transducing sugars may also trigger physiological reflexes independently of sweet-taste perception. Orally applied sugar has long been known to produce a small but marked elevation in plasma insulin levels within minutes, long before the sugar is absorbed in the gut. This cephalic-phase insulin release (CPIR) is documented in rodents and humans, and requires intact taste nerves. CPIR requires vagal stimulation of the pancreas. Insulin release from the pancreas may also be stimulated by glucagon-like peptide 1 (GLP1; also known as incretin), which is secreted by sweet-sensing taste bud cells. Sugar-induced CPIR persists in Tas1r3‑knockout mice and is mediated through the action of KATP channels. Thus, at least two distinct and parallel sugar-sensing mechanisms seem to be initiated in taste buds: one that signals the perception of carbohydrate-rich foods (that is, sweet tastes, via T1R2–T1R3) and one that deploys a physiological reflex of insulin secretion (via a transporter).

Umami
Some amino acids, notably glutamate and aspartate, have a savoury taste named umami. The prototypic stimulus for umami is monosodium glutamate (MSG). Glutamate is abundantly present in meat, fish, cheese and many vegetables. When 5ʹ nucleotides, such as 5ʹ inosine monophosphate (IMP), are present in small amounts alongside glutamate, there is a synergistic augmentation of umami taste. Taste cells detect umami stimuli through multiple receptors. A sizeable amount of literature documents a role bfor T1R1–T1R3 heterodimers in transducing the umami taste. An initial report using Tas1r3‑knockout mice, mice that lack Tas1r1 (which encodes T1R1) and double Tas1r3;Tas1r1‑knockout mice claimed that T1R1–T1R3 heteromers were fully responsible for all umami taste detection. However, studies using an independently generated Tas1r3‑knockout line (see above) showed that the behavioral and neural responses of these mice to umami compounds (MSG and IMP) were nearly normal. Furthermore, a second line of mice in which Tas1r1 was knocked out also demonstrated near-normal responses to umami compounds in taste bud cells and nerves; the only major change was that the nucleotide-mediated augmentation of umami taste was lost41. Thus, it seems that T1R1–T1R3 responds primarily to mixtures of MSG and nucleotides. Umami taste receptors other than T1R1–T1R3 are also present in taste bud cells; these include N‑terminaltruncated, taste-specific variants of the two metabotropic glutamate receptors mGluR4  and mGluR1. Both of these receptors are activated by glutamate at concentrations that are found in foods. Nerve recordings from mice that lack Grm4 (which encodes mGluR4) revealed decreased responses to glutamate and IMP, confirming that a fraction of the afferent nerve response to MSG in wild-type mice is attributable to mGluR4.

Bitter
Bitter taste is stimulated by an enormous variety of compounds that have diverse chemical structures, from simple salts to large complex molecules, many of which are toxic. Bitter-taste receptors (T2Rs) are class A GPCRs, and have short N termini and ligand-binding sites in their transmembrane segments. Unlike T1Rs, the T2Rs are generally considered to function as monomers, although recent evidence suggests that they may also form homodimers and heterodimers. Many mammalian genomes (including the human genome) have 20 or more genes that encode T2Rs; by contrast, only three T1R‑encoding genes have been identified in mammalian genomes. Subsets of T2Rs are co‑expressed in any given bitter-sensing taste bud cell. T1Rs (which detect sweet and umami tastes) and T2Rs are expressed in a non-overlapping pattern, suggesting a separation of receptor cells that detect appetitive versus aversive stimuli. Individual T2Rs in humans and rodents can be narrowly tuned to one or a very few bitter compounds, whereas others are broadly responsive to several bitter chemicals. The breadth of the receptive ranges of human T2Rs has been encyclopedically documented in a thorough study of heterologously expressed taste receptors. This study showed, for instance, that T2R3 responds to only a single compound (out of 94 different natural and synthetic compounds tested), whereas T2R14 responds to at least 33 compounds. Conversely, a single bitter compound often can activate multiple different T2Rs51–54. For example, quinine activates as many as nine different human T2Rs, whereas acetaminophen — an analgesic — stimulates just one human T2R51. This broad and overlapping range of ligand sensitivities of the T2Rs assures that this family of receptors responds to an enormous range of bitter-tasting chemicals (BOX 2). 



Presumably, this redundancy evolved to ensure the detection of potentially toxic (bitter-tasting) chemicals and thus prevent the consumption of harmful foods.

Question: Would organisms not have died, if the distinction of harmful food would not have been detected right from the start ?

An evolutionary note in this context is that orthologous receptors in mice and humans often are responsive to very different bitter tastants, which suggests that receptors have been reassigned to ecologically relevant compounds and that the gene family has been subjected to selective pressures. Many T2Rs exhibit functional polymorphisms that result in varying abilities to taste particular compounds, and these polymorphisms may underlie differences in food preference (BOX 3).



Effector pathways for sweet, umami and bitter taste receptors
In spite of their diversity, T1Rs and T2Rs converge on a common intracellular signalling pathway. These GPCRs all couple to heterotrimeric G proteins that include Gβ3 and Gγ13, as well as Gαgus (also known as gustducin), Gα14 and Gαi . Gα subunits were originally proposed to activate cAMP signalling, but the current view is that they primarily function to regulate Gβγ subunits. cAMP also seems to have a longer-term role by maintaining signalling proteins in a responsive state through protein kinase A activation62. When T1Rs and T2Rs are activated by tastants, Gβγ dimers are released, which stimulates phospholipase Cβ2 to mobilize intracellular Ca2+. Elevated
cytosolic Ca2+ levels lead to the opening of transient receptor potential cation channel subfamily M member 5 (TRPM5), which is a cation-permeable channel that effectively depolarizes taste cells. Interestingly, these same receptors and components of the same signalling pathways are also found in specialized cells in other tissues, where they may detect chemical stimuli without eliciting ‘taste’ per se (BOX 4).

Sour
The proximate stimulus for sour taste is intracellular acidification rather than extracellular protons. Organic (‘weak’) acids, such as citric acid and acetic acid, are more potent stimuli of sour taste than are mineral (‘strong’) acids such as HCl. This is attributed to the greater membrane permeability of the undissociated organic acid molecule and the subsequent generation of protons in the cytoplasm. By contrast, mineral acids readily dissociate in the extracellular solution, but most cell membranes are relatively impermeable to protons. Thus, citric acid and acetic acid are more potent stimuli of sour taste than is HCl when tested at a similar pH. The taste bud cells that depolarize and produce Ca2+ responses to acids are the neuron-like type III cells. Throughout the past two decades, numerous plasma membrane ion channels have been proposed as transducers for sour taste, including epithelial Na+ channels (ENaCs)69, hyperpolarization-activated cyclic nucleotide-gated channels and acid-sensing ion channels (ASICs). More recently, two members of the TRP superfamily of ion channels — polycystic kidney disease protein 1‑like 3
(PKD1L3) and PKD2L1 — were proposed as the major transducers of sour taste. However, all of these candidates have been ruled out as sour taste transducers either because they lacked biophysical characteristics that were
consistent with sour-evoked responses in taste cells, or because mice in which the candidate receptor-encoding genes were knocked out retained all or most of their sensitivity to sour tastants. Confocal imaging of pH and Ca2+ has shown that organic acids permeate type III cells, acidify the cytoplasm and block leak K+ channels to depolarize the cell membrane. These leak channels have recently been identified; specifically, type III cells express an inwardly
rectifying K+ channel, KIR2.1, which is inhibited by intracellular protons. Extracellular protons, such as those contributed from mineral acids or from dissociated organic acids, pass through a proton conductance that seems to be concentrated to the apical tips of type III cells. The molecular identity of the proton channel that is responsible for this proton movement remains to be established. The influx of protons through the channel generates a small depolarizing current, and furthermore, the accumulation of protons inside the cell contributes to the inhibition of KIR2.1 channels. The net result in both cases is depolarization of the type III sour-sensing cells such that they reach the threshold for action potential initiation.

Salty
The taste of NaCl is still somewhat of an enigma. Animals and humans readily consume NaCl below isotonic concentrations (that is, concentrations below approximately 150 mM). This appetite is presumably to ensure the adequate ingestion of an essential mineral. By contrast, higher concentrations of NaCl are normally aversive, which presumably reflects a survival mechanism that protects individuals against hypernatremia and dehydration. It remains unclear exactly which taste bud cells transduce NaCl and what the transduction mechanisms are. Some of the key observations in this context are that, in rodents, amiloride, a diuretic, decreases the amplitude of responses to NaCl in afferent nerve recordings and reduces the behavioral response (licking) to NaCl solutions. Yet, amiloride does not seem to change the perception of the saltiness of NaCl in humans. In rodents, amiloride affects neural responses mainly to NaCl; the effect on other salts is less consistent. The dampening of NaCl taste by amiloride has long been interpreted as evidence for the essential role of the amiloride-sensitive Na+ channel ENaC in salty taste. Fungiform taste bud cells loaded with a Ca2+ indicator have been reported to respond to apically applied NaCl7. When the gene encoding the obligatory α-subunit of ENaC was conditionally knocked out in taste cells, neural responses and the ability of mice to respond behaviourally to NaCl were lost7. These data confirmed earlier interpretations that ENaC is necessary for salty taste detection in rodents. However, no evidence has yet directly demonstrated that ENaC is the principal salt receptor in humans. In a subsequent study, the authors reported that the signals for low (preferred) concentrations of NaCl originated in amiloride-sensitive taste bud cells, whereas high (aversive) NaCl concentrations were detected by completely separate amiloride-insensitive taste bud cells. They further inferred that the two cell types transmitted their signals along separate afferent neurons. However, Ca2+ imaging subsequently showed that the amiloride sensitivity of afferent neurons was similar regardless of their NaCl sensitivity; that is, high-NaCl versus low-NaCl sensitivity did not covary with amiloride sensitivity. To date, the identity of the taste bud cells that sense NaCl is not known. Amiloride-sensitive Na+ currents have been reported in taste bud cells that are neither type II or type III cells, based on their lack of voltage-gated currents82. By contrast, a report from another group demonstrated that the amiloride-blocked resting conductance was most prominent in cells that had the characteristics of type II cells. Neither of these studies pinpointed the ENaC-mediated currents to cells that could be identified by type-specific molecular markers. Yet other reports assign amiloride-insensitive responses to NaCl to acid-sensing type III cells80,84. This is an area ripe for clarification.

Fat
Dietary fats consist largely of triglycerides. Solid fats and oils differ in the length of the fatty acid chains of the triglyceride and the number of unsaturated positions. Most animals have a well-developed preference for fats. The sensations evoked by dietary fats most certainly include somatosensory components such as texture and viscosity. Whether fats stimulate a gustatory component remains debated. Rats lose their ability to detect and identify certain fats if the innervation of their taste buds is interrupted, which supports a role for taste buds in sensing fats. The principle argument against fat as a taste quality is that triglycerides have not been shown to stimulate taste cells. However, oral lipase activity in rodents rapidly and effectively digests fats into free fatty acids in the immediate environment of taste buds. Fatty acids themselves are effective taste stimuli. In humans also, oral lipase activity is detectable but only at low levels, leaving its role in fat detection unresolved. There may not be a singular fat taste quality, as dietary free fatty acids evoke multiple orosensations — including ‘fatty’ and ‘irritating’— depending on chain length and concentration. One of the earliest studies on fat taste reported that certain polyunsaturated fatty acids act directly on K+ channels, resulting in the prolonged depolarization of taste bud cells. More recently, receptor-mediated mechanisms have been documented, including roles for a transporter for fats, CD36 (also known as platelet glycoprotein 4), and two GPCRs, GPR40 and GPR120 (also known as free fatty acid receptors 1 and 4, respectively). CD36 was reported to be localized to the apical tips of some taste bud cells and to elicit elevations in intracellular Ca2+ levels when stimulated by fatty acids. How the transporter couples to Ca2+ signalling is not yet known. Intriguingly, oral stimulation of CD36 by certain fatty acids elevates pancreatic secretions — which is suggestive of a ‘cephalic phase response’, preparing the gut for digesting lipids. GPR120 is expressed in a subset of rodent type II cells and, when activated, mobilizes Ca2+, as is the case for T1R and T2R activation. GPR120 seems to be distributed and function similarly in human taste buds. In mice, knocking out the gene that encodes CD36, GPR40 or GPR120 results in partial deficits in fat taste92,94. In short, fat taste is complex, and no particular transduction mechanism has been unambiguously identified. Indeed, several transducer proteins may interact to generate the taste of fat. Aside from the basic taste qualities discussed above — sweet, bitter, salty, sour and perhaps fatty — additional tastes have been described

Neurotransmitters and modulators
At least five neurotransmitters have been identified in taste buds. Their release and possible roles in taste have been examined in detail, and are discussed below. In addition, several peptides that function as hormones or neuromodulators interact with the taste system by influencing the sensitivity or the output of taste buds. As the topic of the role of peptides in taste has been reviewed recently, we focus here on small-molecule transmitters. ATP. Early suggestions that ATP is a transmitter for taste buds were based on immunostaining for P2X purinoceptors in nerves associated with taste buds in rat tongues. A role for this transmitter in taste signaling was validated in a study showing that sheets of lingual epithelium containing taste buds secreted ATP when stimulated with bitter tastants. Furthermore, when the genes that encode the purinoceptors P2X2 and P2X3 were knocked out, mice became taste-blind to sweet, salty, bitter and umami.

The endocrinology of taste receptors 2

Chemosensory processes in the tongue
Taste bud cell types and taste perception
Taste, or gustation, is one of the five primary senses. Taste perception is triggered by chemicals when they come in contact with taste bud cells (TBCs) of the tongue; subpopulations of TBCs synthesize hormones (such as GLP‑1 and ghrelin) that are also found in the gut and brain. Five basic tastes are recognized by most animals (sweet, umami, bitter, salty and sour) and there is growing evidence that fat can also be tasted. Taste buds have a structure similar to that of a garlic bulb (Figure 1a) and they primarily reside within taste papillae located in circumvallate, foliate and fungiform papillae of the tongue (Figure 1b). 











Some isolated taste buds chemosensory cells that express G-protein-coupled taste receptors (taste GPCR) are present on the palate, epiglottis, pharynx, larynx and the nasoincisor duct of rats. Each taste bud contains ~50–100 TBCs (assembled as ‘cloves’ in the garlic-bulb-like structure) that are of epithelial origin, unlike olfactory receptor cells that arise from neurogenic precursors. TBCs are classified into four subtypes and all taste buds contain cells of all four subtypes regardless of their anatomical location (Figure 1a).

Type I cells
Approximately 50% of the total number of TBCs are type I cells that maintain the supporting structure of the taste buds. These cells are characterized by distinct electrophysiological features. Type I TBCs have small voltage-gated outward K+ and inward Na2+ currents but no voltage-gated Ca2+ currents. Amiloride-sensitive sodium channel subunit α (commonly known as epithelial sodium channel subunit α [α‑ENaC]) is expressed on type I cells and is considered to be the major mediator of perception of low salt (for example, NaCl or KCl). TBC-specific deletion of α‑ENaC in mice caused complete loss of behavioral attraction to salt; however, the downstream signaling mechanisms that are activated when a low-salt tastant engages type I cells and how these cells communicate with nerve fibers are unknown. In addition to expressing α‑ENaC, these cells express membrane-bound ATPase on the cell surface that degrades ATP released from neighboring cells. Type I cells have extensive lamellar processes that wrap around the other cell types within the taste bud structure, which probably function to control the dissipation of cell signaling molecules throughout the taste bud and isolate ion fluctuations to specific areas of the taste bud.


Type II cells
Type II cells, often referred to as receptor cells, express receptors for sweet, umami and bitter tastants. Sweet and umami tastants are sensed by heterodimeric GPCR comprising a family of three receptors (TAS1Rs): taste receptor type 1 member 1 (TAS1R1), taste receptor type 1 member 2 (TAS1R2) and taste receptor type 1 member 3 (TAS1R3). Heterodimeric receptors of TAS1R1 and TAS1R3 subunits are activated by umami tastants (for example, glutamate, broth, mushrooms, meat and l‑amino acids) and heterodimeric receptors of TAS1R2 and TAS1R3 subunits are activated by sweet tastants (for example, sucrose, fructose and glucose, as well as artificial sweeteners such as sucralose).Mice that lack TAS1R3 have diminished responses to both sweet and umami tastes, which indicates that although these heterodimeric complexes might be the major mediators for these tastes, other mechanisms for sweet and umami taste perceptions exist. Bitter tastants (such as caffeine, quinine and denatonium benzoate) are sensed by GPCR of the type 2 taste receptor (TAS2R) family, which has ~30 members. Each type II TBC expresses either the TAS1Rs or specific members of the TAS2R family (each bitter-tasting cell can co-express 4–11 TAS2Rs) and, therefore, responds exclusively to either sweet and umami, or bitter tastants. Type II cells contain the bulk of the different hormones synthesized by TBCs, as well as their cognate receptors (Figure 2). Expression of fat sensors, such as free fatty acid receptor 4 (GPR120) and platelet glycoprotein 4 (CD36), which detect long-chain fatty acids (LCFAs), in type II TBCs has been reported (Figure 2).



CALHM1 is a voltage-gated ion channel that mediates tetrodotoxin-sensitive ATP release in taste buds (Fig. 4l) as an essential mechanism of sweet, bitter and umami taste perception. As such, CALHM1 provides a missing link in the signal-transduction cascade in type II cells, connecting taste receptor activation and the generation of Na1 action potentials to the activation of afferent gustatory neural pathways1 (Fig. 4m). 9



Type III cells
Presynaptic cells (type III cells) are the only type of TBCs that form conventional neuronal synapses with sensory afferent intragemmal nerve fibres. Similar to neurons, these cells contain voltage-gated Ca2+ channels and release vesicular serotonin, acetylcholine, norepinephrine and γ‑aminobutyric acid (GABA) when depolarized. These cells also express polycystic kidney disease 2‑like 1 protein (PKD2L1) and polycystic kidney disease 1‑ like 3 protein (PKD1L3) channels, which together are involved in perception of sour (acid) taste. The absence of PKD2L1-expressing type III cells in mice caused either complete abolition of the response or reduced sensitivity to acidic chemicals (such as citric acid). High salt concentrations are aversive and activate bitter sensing in type II cells and sour sensing in type III cells.

RECEPTOR PROTEINS FOUND IN TASTE CELLS 10

SWEET -- Sugars and artificial sweeteners are detected by T1R2 and T1R3 heteromers, UMAMI --T1R1 and T1R3 GPCRs combine to form a broadly tuned L-amino-acid receptor
BITTER-- Bitter chemicals are detected by 30 T2R receptor family members.
SOUR -- Acids are detected by PKD1L3- and PKD2L1 sour-sensing cells .
SALT -- Not known although approximately 20% effect may be by amiloride-sensitive sodium channels.
FAT -- Speculative -- CD36 Receptor


Taste cell precursors
The final subtype of TBCs (previously referred to as type IV cells) comprise a small heterogeneous group of cells located toward the base of the taste bud structure. These cells were initially thought to be the exclusive progenitor cells for the differentiated TBC types; however, it is no longer thought that the TBC stem cell niche is located solely at the base of the taste bud. Sonic hedgehog protein (SHH) regulates the differentiation of TBCs. SHH-expressing cells within taste buds signal to SHH-responsive cells, which are located outside of the taste bud and express the transcription factors zinc finger protein GLI1 and patched domain-containing 1 (known as patched 1). Multiple areas of SHH-responsive cells surround taste buds in the adult mouse tongue. Using lineage-tracing experiments, SHH-expressing cells within taste buds were shown to be immediate precursors of the other three cell types. Additionally, another study confirmed that the progenitors of TBCs are located outside of the taste bud itself by showing that very few (<10%), if any, cells proliferate within taste buds. Thus, the small cells present at the base of taste buds are of two different categories, quiescent precursor cells and immature taste cells, neither of which are progenitor cells. Therefore, the term type IV cell is no longer commonly used to describe a particular TBC type.

Signalling mechanisms of taste perception
Given that type III cells are the only taste cells with conventional neuronal synapses (Figure 1a), type II and type III cells were previously thought to communicate via gap junctions to elicit activation of taste nerves to convey information to the brain regarding the nature of the tastant. In transgenic mice that express a fluorescently labeled trans-synaptic protein (wheat germ agglutinin; WGA) under the control of the TAS1R3 promoter, some WGA expression was found in serotonin-positive cells (presumably type III cells), which implied direct communication and passage of proteins from type II cells. However, two subsequent publications did not find lateral transfer of non-fluorescently labeled WGA linked to TAS1R3 in type III cells. Correspondingly, transgenic mice expressing WGA under the control of the PKD1L3 promoter, which is only expressed in type III cells, did not have any WGA present in type II cells. These data suggest that no direct transfer of protein occurs between type II and type III cells. Furthermore, genetic ablation of type III cells from mice does not result in disruption of sweet, bitter or umami perception, which demonstrated that these cells are not required for transmission of taste information from type II cells.

Studies published in the past decade have shown that type II cells directly communicate with taste nerves via ATP release and activation of purinergic receptors on nerve fibres, thereby negating the need for direct transfer of molecules between the two cell types. In addition to ATP, type II cells release locally produced hormones for communicating information to neighbouring cells (paracrine effect). These hormones can also alter taste perception in an autocrine fashion, by modifying taste signalling mechanisms in the hormone-expressing cells. In addition, the afferent nerve fibres in taste buds contain receptors for locally produced hormones, such as GLP‑1 and neuropeptide Y (NPY), thereby enabling modulation of the intensity of the taste signal that acts as an ‘on switch’ for downstream cell signalling after exposure to a particular tastant (Figure 2). TAS1Rs (umami and sweet), TAS2Rs (bitter) and fat receptors share downstream signalling pathways, albeit in different subtypes of TBCs, that ultimately lead to release of ATP and hormones. 

Specifically, when a tastant (sweet, bitter, umami or LCFAs) binds to its specific taste receptor or sensor, PLCβ2 is activated and second messengers such as IP3 are generated. IP3 causes release of intracellular Ca2+ that gates TRPM5 (transient receptor potential cation channel subfamily M member 5; encoded by Trpm5) channels, which results in cellular depolarization. The action potentials generated in the TBCs lead to release of non-vesicular ATP through voltage-gated CALMH1 (calcium homeostasis modulator 1) channels that engage purinergic receptors on the sensory nerve fibres, as well as on type II and type III cells. In type II cells, activation of purinergic receptors potentiates increased release of ATP, whereas in type III cells, voltage-gated Ca2+ channels are activated, which causes release of classic neurotransmitters. Knockout of Trpm5 in mice abolished sweet, bitter and umami discrimination and Trpm5 was also found to be required for LCFA-mediated depolarization of TBCs and a preference in mice for fat over non-fat-containing tastants. Knockout of CALHM1 in mice led to severely impaired perception of sweet, umami and bitter tastes, as well as a strong reduction in release of ATP from type II TBCs in response to tastants. Together, these observations suggest that the major line of communication of taste information from type II cells to the brain occurs via release of ATP, which interacts directly with the taste nerves to convey information to higher order neurons. Importantly, the ATP that is released from type II cells is degraded by membrane-bound ATPases on type I cells, which generates ADP that prevents purinergic receptor desensitization on afferent fibres. Non-specific ectopeptidases degrade some ADP molecules to adenosine that can act on adenosine receptor A2B, which is present on a subset of TAS1R-expressing cells and enhances ATP release (and presumably also increases hormone release) in response to activation of TAS1Rs by sweet-tasting ligands.Sour taste is perceived when protons enter type III cells, causing cellular acidification. This proton influx results in closure of resting K+ channels, membrane depolarization and release of classic neurotransmitters.

Neuronal control of taste
Taste sensation is bilaterally represented in the brain. Cranial nerves VII (facial), IX (glossopharyngeal) and X (vagus) convey taste information through multiple relay stations that ultimately connect to the primary taste cortex (located in the insula, which is overlaid by the opercular cortex). Nerve fibres from the cranial nerves enter the ipsilateral nucleus of the solitary tract (NTS) in the medulla. In rodents, NTS efferent fibres convey taste information to gustatory centres of the parabrachial nucleus (PBN) in the pons that synapse with neurons in the thalamus (Figure 4). In primates, NTS fibres bypass the PBN and synapse directly with thalamic neurons. In both rodents and primates, thalamic afferents project to the insula. In turn, the taste cortex sends projections to the amygdala and onwards to the lateral hypothalamus and nucleus accumbens, where dopamine is released in response to hedonic reward stimuli. At or just above the PBN, one-third of the ascending nerve fibres carrying taste perception from the tongue cross and ascend bilaterally to the thalamic taste area, thereby allowing for bilateral taste representation in the brain. The NTS is an important site of convergence for gustatory fibres from all three cranial nerves transmitting taste information, autonomic efferent and afferent fibres from the gut, and somatosensory afferent fibres from the face, mouth and tongue via cranial nerve V (the trigeminal nerve). In addition, local projections from the NTS control salivation rates within the mouth, which is necessary for mastication and appreciation of food. Salivation is highly activated when sour tastants are present in the mouth. Von Ebner’s glands, innervated by the glossopharyngeal nerve, secrete serous material containing lipases into the moats of the circumvallate and foliate papillae, which enables release of free fatty acids (the ligands for GPR120 and CD36) from masticated food.

Neurotransmitters and Cell-to-Cell Communication in Taste Buds 3
Recent studies have identified neurotransmitters released by taste buds and, by so doing, have revealed which cells secrete which transmitter(s) and how the transmitters activate the taste bud circuits.

Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission. They transmit signals across a chemical synapse, such as a neuromuscular junction, from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell.[1] Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, where they are received by receptors on the target cells. 4

Related studies have also revealed how the different types of taste bud cells respond to chemical stimulation. Receptor (Type II) and presynaptic (Type III) cells have been shown to be the principal players in chemosensory stimulation. Isolated receptor cells respond mainly to a single taste quality — sweet, bitter, or umami — and not to combinations. This is consistent with the selective expression of taste GPCRs in these cells. In contrast, isolated
presynaptic cells respond mainly to KCl depolarization and to sour (acid) taste stimuli. In situ, however, presynaptic cells appear to respond to stimulation from multiple taste categories, including sweet, bitter, salty, umami, and sour. This discrepancy between responses in isolated presynaptic cells and presynaptic cells in situ stems from the presence of cell-to-cell communication within taste buds. Cell-to-cell communication in taste buds was initially proposed based on ultrastructural studies on fish taste buds and then demonstrated with intracellular recordings in amphibian taste buds. However, the full details have only recently been learned from investigations using biosensor cells and confocal Ca 2 + imaging in lingual slices from mouse vallate taste buds. These studies have revealed that upon taste stimulation with bitter, sweet, or umami substances, receptor cells secrete adenosine triphosphate (ATP). Taste-evoked ATP acts on three postsynaptic targets: P2X2 and P2X3 receptors expressed on gustatory primary afferent fibers ; (2) P2Y receptors (probably P2Y4) on presynaptic cells in close vicinity to the activated receptor
cells; and  P2Y1 autocrine receptors on receptor cells. All these actions are excitatory. A robust ecto-ATPase (NTPDase 2) is expressed on the glial-like Type I taste bud cells. NTPDase 2 serves to terminate the postsynaptic actions of ATP by degrading the purine to adenosine diphosphate and, to a lesser extent, adenosine monophosphate. Taste-evoked excitation of receptor cells thus secondarily activates presynaptic cells via ATP. Presynaptic cells, in turn, secrete serotonin (5 hydroxytryptamine, or 5-HT) and norepinephrine (NE). Postsynaptic targets for these aminergic transmitters are not well characterized, especially for NE. However, 5-HT exerts a strong negative feedback
onto receptor cells. 5-HT inhibits receptor cells and diminishes their ability to secrete ATP. Blocking 5-HT1A receptors relieves this inhibition and leads to a striking enhancement of taste-evoked ATP secretion.
These interactions are summarized in Figure 26.1 .




Interestingly, the mechanisms involved in the synaptic release of ATP and 5-HT in taste buds are quite unusual. First, receptor cells secrete ATP via pannexin 1 gap junction hemichannels. These gap junction hemichannels are believed to be opened by the combined action of intracellular Ca 2 + release (from activation of taste GPCRs) and membrane depolarization (from calcium-activated TRPM5 cation channels) ( Fig. 26.2 ).



This novel extra synaptic secretory mechanism explains why conventional ultrastructural features of synapses, including clusters of synaptic vesicles and synaptic membrane thickenings, are absent on receptor cells. It is not
known whether there are focal sites for taste-evoked ATP secretion or whether ATP secretion is broadly dispersed across the basolateral membrane of the receptor cell. Release of 5-HT and NE appears to be more conventional insofar as secretion of both these biogenic amines can be triggered by membrane depolarization and Ca 2 + influx, the usual mechanism for vesicular exocytosis. Further, 5-HT and NE are coreleased in some cases.
However, 5-HT secretion can also be triggered in the absence of Ca 2 + influx by activating intracellular Ca 2 + release, indicating that there are at least two different modes for secretion of this amine. Whether this latter mechanism, secretion triggered by Ca 2 + released from intracellular stores, is vesicular has not been investigated. Precisely how feedforward excitation of ATP onto presynaptic cells, feedback (autocrine) excitation of ATP onto presynaptic cells, and negative feedback (paracrine) exerted by 5-HT from presynaptic onto receptor cells work together to encode taste qualities and shape signals in the peripheral sensory organs of gustation remains to be worked out in detail. It is clear, however, that cell-to-cell signaling takes place during taste stimulation and that purinergic and aminergic transmitters are involved. The functional organization of taste buds thus can be understood as (a) “labeled” receptor cells (not lines); (b) convergent input onto presynaptic cells (several receptor cells may converge onto a single presynaptic cell); and (c) some extent of feedback (autocrine and paracrine) signal processing. Interestingly, manipulating peripheral circulating levels of 5-HT and NE affects human taste thresholds, supporting the role of biogenic amines in modulating peripheral gustatory mechanisms. We and others are investigating the details of signal processing in taste buds and determining whether other neurotransmitters and neuromodulators are involved.

Taste coding
How information from taste buds is transmitted to the central nervous system ( CNS )  (specifically to neurons in the nucleus of the solitary tract) and, in particular, how signals discriminating sweet, sour, salty, bitter, umami and possibly other tastes are encoded are thorny questions. 









There has been more than 75 years of heated debate over these issues. At one extreme is the labelled-line coding model, which states that individual taste bud cells exclusively identify a unique taste quality (for example, sweet taste) and synapse with afferent fibers that are dedicated to that quality. Moreover, the central projections of the afferent neurons are ‘labelled’ by that same taste quality and synapse with dedicated hindbrain neurons that relay the information for that one quality to higher brain centers, thereby establishing a ‘labelled line’ of transmitted information. An early suggestion of labelled-line coding in the periphery came from single-unit recordings in rodents, which showed that individual fibers respond best to one taste quality (for example, “NaCl-best”), although activity was also elicited by tastants of other qualities. Studies on a number of other types of mammal have shown that sweet-responsive fibers are particularly well-tuned to sugars and artificial sweeteners.  

The expression patterns of taste receptors in taste buds lend strong evidence for taste quality distinction at the level of taste cells. T2Rs, which detect bitter stimuli, are not found in cells that express T1Rs, which detect sweet or umami stimuli. Moreover, sour-sensing cells are a separate cell type from both T1R‑expressing and TR2‑expressing cells. Furthermore, the genetic ablation of only type III cells results in the loss of sour taste, as observed both at the behavioral level and in afferent recordings. In addition, the expression of a modified opioid receptor — receptor activated solely by a synthetic ligand (RASSL) — in T1R‑expressing cells drives behavioral preference for a compound that normally has no taste: namely, the synthetic opioid spiradoline. Conversely, the expression of RASSL in T2R‑expressing cells resulted in an aversion to spiradoline. The implication is that sweet and bitter ‘labels’ are resident in particular cells; activating the afferent fibers that innervate these cells would thus result in stereotypical responses, consistent with labelled-line coding. An alternative model for how taste is encoded in the periphery states that information is transmitted by combinatorial activity in multiple peripheral afferent fibers (FIG. 2).



According to this model, ensembles of dissimilar afferent fibers are activated by a taste stimulus. The overall combination of fibers activated encodes the taste quality, such as sweet. Indeed, such combinatorial coding has long been established for color vision and characterizes odor recognition in the olfactory system. Strong evidence for the combinatorial coding of peripheral taste comes from several lines of experimentation. First, taste buds contain both narrowly tuned cells and more broadly responsive ones. Specifically, separate populations of type II cells respond mainly to a single taste quality (for example, sweet or bitter). By contrast, type III taste bud cells respond directly to sour stimuli and indirectly (via cell–cell communication) to multiple taste stimuli. Second, there are decades of electrophysiological recordings from individual sensory neurons that innervate taste buds in animals ranging from rodents to primates. Many of these recordings have revealed the existence of highly tuned neurons — which are also referred to as ‘specialists’ — that respond overwhelmingly only to stimuli of one taste quality. However, these same recordings also reveal neurons — called ‘generalists’ — that respond to two or more different taste qualities. The relative proportions of such specialist and generalist neurons vary substantially depending on the species, the choice of stimuli presented and the concentration of the stimulus. Often, one taste stimulus is most efficacious for a given neuron (for example, “sucrose-best”, but even that property is not always fixed. Specifically, increasing the concentration of tastant-containing solutions (that is, increasing the stimulus strength) converts seemingly narrowly tuned neurons into broadly responsive ones, and neurons with one best stimulus at low concentration acquire a different ‘best stimulus’ at higher concentrations. These observations are inconsistent with the fixed, labeled line model of taste coding. A third possibility is that taste qualities are encoded by different temporal patterns of activity in gustatory neurons. Although temporal coding has been implicated in brainstem and cortical gustatory centres, there is no evidence that information in peripheral sensory neurons is encoded by spike timing. Indeed, an early study showed that stimulating human taste buds with a train of electrical pulses evoked a taste sensation that did not change when the stimulus rate was altered. However, this study did not test different patterns of electrical stimulation. Taste coding in central taste pathways is beyond the scope of this Review and has been comprehensively reviewed elsewhere. It suffices to say, however, that the three models — labelled-line coding, combinatorial processing, and temporal patterning — continue to be raised as explanations of how taste is encoded in higher brain centers, including the primary gustatory cortex.

Conclusions
Until recently, many researchers thought that questions underlying the cellular and molecular mechanisms of the basic taste qualities had been settled. This Review explains that although we indeed understand many of the receptors and transmitters that are involved in detecting sweet, sour, salty, bitter and umami tastes, major gaps in our knowledge remain. Issues awaiting resolution include the molecular identity of additional signalling pathways for detecting umami and sweet tastes; the cells involved in detecting salty tastes; whether ‘fatty’ is a basic taste; the role of cell–cell communication in taste buds; and, more broadly, how distinct taste qualities are encoded in sensory afferent fibres and beyond following their initial detection in the taste bud.

Common Sense about Taste: From Mammals to Insects 5
The sense of taste is a specialized chemosensory system dedicated to the evaluation of food and drink. Despite the fact that vertebrates and insects have independent, distinct anatomic and molecular pathways for taste sensation, there are clear parallels in the organization and coding logic between the two systems. There is now persuasive evidence that tastant quality is mediated by labeled lines, whereby distinct and strictly segregated populations of taste receptor cells encode each of the taste qualities.

Unlike touch, vision, audition, or olfaction, which function in diverse behavioral contexts, the sense of taste has evolved to serve as a dominant regulator and driver of feeding behavior. Gustatory systems detect nutritionally relevant and harmful compounds in food and trigger innate behaviors leading to acceptance or rejection of potential food sources. Taste is, therefore, a powerful system in which to ask the question, how is sensory input transformed and distributed to evoke a specific behavioral output? The first step in this endeavor is to define how tastant identity and concentration are translated into patterns of activity by primary receptor cells.

Taste Receptor Cells Are Hardwired to Behavioral Output
The expression of bitter, sweet, umami, and sour receptors in segregated TRCs implies that these tastes are mediated by distinct, dedicated receptor cells, each tuned to a single taste modality (Figure 3). Indeed, a series of studies in genetically engineered mice have now substantiated this logic of taste coding and provided definitive evidence of a labeled-line organization for the taste system at the periphery. For example, specific taste receptor cell populations can be genetically ablated by expression of the diphtheria toxin alpha subunit, and the resulting animals exhibit a deficit only in that modality while other responses remain intact. In addition, the innate nature of taste preferences strongly suggests that TRCs are hardwired to behavioral programs for acceptance and rejection. If this is true, activation of selective TRC populations should be sufficient to drive taste behavior. For example, expression of a blue light receptor in sweet cells should, in principle, make blue light “taste” sweet. Although this experiment has not been done yet, expression of a non-taste receptor in sweet or bitter TRCs did allow taste cells to be activated, and a strong specific behavior elicited, by an ordinarily tasteless ligand. As Figure 4 shows, if this receptor is expressed in sweet-sensing cells under the control of the T1R2 promoter, these mice are strongly attracted to solutions containing the normally tasteless ligand . If, on the other hand, the very same RASSL receptor is expressed in bitter cells, these mice now exhibit strong repulsion. Similarly, expression of a bitter receptor in sweet-sensing cells produces animals that exhibit strong attraction to the cognate bitter ligand, that is, bitter tastes sweet. These behaviors do not involve learning, as receptor expression is absent during development and is induced only immediately prior to the behavioral tests. Taken together, these experiments demonstrate that behavioral responses to taste stimuli are determined by the identity of the stimulated cell type, and not by the properties of the taste receptor molecule or even the tastants; they also illustrate how the functional segregation of taste modalities endows the taste system with a refined engine to drive innate behaviors. It will be an interesting challenge to understand the genetic program and mechanism(s) by which each taste cell type is hardwired to the appropriate neural circuitry and to explore if one can also alter taste behavior by manipulating the wiring scheme.

The neural representation of taste quality at the periphery 6
To understand how TRCs transmit information to higher neural centres, we examined the tuning properties of large ensembles of neurons in the first neural station of the gustatory system. Here, we generated and characterized a collection of transgenic mice expressing a genetically encoded calciumindicator2 in central and peripheral neurons, and used a gradient refractive indexmicroendoscope3 combined with high-resolution two-photon microscopy to image taste responses from ganglion neurons buried deep at the base of the brain. Our results reveal fine selectivity in the taste preference of ganglion neurons; demonstrate a strong match between TRCsin the tongue and the principal neural afferents relaying taste information to the brain, and expose the highly specific transfer of taste information between taste cells and the central nervous system.

In mammals, taste receptor cells are assembled into taste buds that are distributed in different papillae in the tongue epithelium. Taste buds are innervated by afferent fibers that transmit information to the primary taste cortex through synapses in the brainstem and thalamus. In the simplest model of taste coding at the periphery, each quality, encoded by a unique population of TRCs expressing specific receptors (for example, sweet cells, bitter cells, and so on), would connect to a matching set of ganglion neurons. Notably, althoughTRCs are tuned to preferred taste qualities, the nature of their functional ‘handshake’ with the nervous system has been a matter of significant debate. We reasoned that this fundamental question could now be resolved by directly examining the tuning properties of taste ganglion neurons. We focused on the geniculate ganglion ( see Fig.33.12 below ), as its neurons innervate all taste buds in the front of the tongue and palate1, and opted to use two-photon calcium imaging to monitor tastant-evoked neural activity in vivo.



 This strategy, however, required the solution of two technical challenges: first, the ganglion is located in a bony capsule under the brain, some 4mm from the surface, far beyond the reach of conventional microscopy; and second, geniculate ganglion neurons would have to be loaded with sensors of neuronal activity that can report function with good temporal, spatial and dynamic range.To solve the first challenge, we implemented the use of two-photon microendoscopy, where a gradient refractive index (GRIN) lens is used as an optical extension device. The GCaMP family of genetically encoded calciumsensors are an attractive tool to solve the challenge of indicator loading, yet there were no suitable mouse lines or drivers appropriate for targeting geniculate ganglion neurons. Therefore, we generated a collection of 40mouse lines expressing GCaMP32 driven by Thy1 (Fig. 1a), a neuronal promoter highly
sensitive to position effects, and screened for those that express the sensor in most geniculate ganglion neurons (Fig. 1b).



Line 1 had essentially complete labeling of geniculate ganglion neurons (Fig. 1c), and stimulation of the ganglia ex vivo produced reliable calcium-dependent fluorescence changes (Fig. 1d). To take advantage of the more recent versions ofGCaMP, we subsequently developed a viral infection approach that efficiently labels geniculate ganglion neurons via retrograde transfer of the virus from their terminal fields in the nucleus of the solitary tract (see Methods for details). A key prediction of our findings is the expectation that responses to taste mixes should largely reflect the sum of the responses to the individual tastants (that is, as dedicated lines operating independently of each other). Therefore, we tested the representation of binary mixes relative to the responses to the individual components.We chose three pair sets including sweet, bitter, sour and salt tastes and examined their responses. Our results (Extended Data Fig. 6) demonstrate that taste mixes indeed behave like the simple addition of the responses to the individual tastants. This study also illustrates and uncovers three additional aspects to the representation of taste in the first neural station. First, it reveals that although there are 26 possible combinations of ‘multi-tuned’ responses (10 doubles, 10 triples, 5 quads and 1 that may potentially respond to all five classes of taste), only small numbers of bona fide multi-tuned neurons are found at over 1%. Second, half of the apparently multi-tuned ganglion neurons belong to just one class, namelybitter–sour.And third, umami-responding neurons are divided between umami-alone and umami–sweet responders.

7




The gustatory cortex and multisensory integration 8
The central gustatory pathways are part of the brain circuits upon which rest the decision to ingest or reject a food. The quality of food stimuli, however, relies not only on their taste but also on properties such as odor, texture and temperature. We will review anatomical and functional evidence showing that the central gustatory system, in particular, its cortical aspect, functions as an integrative circuit where taste-responsive neurons also display sensitivity to somatosensory and olfactory stimulation. In addition, gustatory pathways are modulated by the internal state of the body, with neuronal responses to tastes changing according to variations in physiological parameters such as gastrointestinal hormones and blood glucose levels. Therefore, rather than working as the receptive field of peripheral taste receptor cells, the central gustatory pathways seem to operate as a multisensory system dedicated to evaluate the biological significance of intra-oral stimuli.

When are we constantly and simultaneously bombarded with various types of sensory inputs, which brain mechanisms allow us to deal with the world in a meaningful manner? The problem of multisensory integration essentially refers to the set of brain processes involved in integrating incoming sensory inputs from several modalities, allowing for the formation of unified perceptual objects and consequently for appropriate behavioral responses to be generated. In many cases, survival of an organism depends on appropriate responses to multisensory stimuli. Selecting foods for ingestion is a clear instance of a multisensory problem that must be solved, promptly and correctly, by any organism. In fact, the placing of food in the mouth simultaneously generates taste, olfactory and somatosensory (texture, temperature) inputs to the central nervous system. Once a stimulus is inside the oral cavity, the decision to ingest or reject it will depend on the evaluation of its multisensory aspects given that not only taste but also other attributes such as odor and consistency, will function as cues to the nutritive value or potential toxicity of the stimulus.

Which brain regions control ingestive behaviors based on these multiple, simultaneous sensory inputs from the oral cavity and viscera? Much progress has been made recently on unveiling both the peripheral and central mechanisms of gustation. One pattern emerging from these recent findings concerns the sensitivity of the central gustatory pathways to multiple sensory inputs arising from the oral cavity.  In fact, both electrophysiological and functional neuroimaging studies make a strong case in favor of the hypothesis that the functions of the gustatory cortex are not restricted to reflecting taste receptor activity. In what follows, we will review evidence of multisensory responses in GC and propose that this primary sensory cortical region works as an integrative circuit, having the capability to encode multiple physical-chemical attributes of stimuli placed in the oral cavity.

1. http://www.nature.com.ololo.sci-hub.cc/nrn/journal/vaop/ncurrent/full/nrn.2017.68.html
2. http://www.nature.com.ololo.sci-hub.cc/nrendo/journal/v11/n4/abs/nrendo.2015.7.html
3. Handbook of Brain microcircuits, page 279
4. https://en.wikipedia.org/wiki/Neurotransmitter
5. http://www.cell.com.sci-hub.cc/abstract/S0092-8674(09)01249-5
6. http://www.nature.com.sci-hub.cc/nature/journal/v517/n7534/full/nature13873.html
7. http://www.nature.com.sci-hub.cc/nature/journal/v444/n7117/full/nature05405.html
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726647/
9. http://www.nature.com.sci-hub.cc/nature/journal/v495/n7440/full/nature11906.html
10. http://www.edinformatics.com/math_science/science_of_cooking/taste_molecules.htm

An Evolutionary Perspective on Food and Human Taste
Our particular history, beginning as ape-like creatures millions of years ago living in tropical forests and ending with a global dispersion of humans to every known climate and environment, has resulted in our specific taste abilities and preferences for sweet, sour, salty, fatty, umami, and starchy foods.



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The neural mechanisms of gustation: a distributed processing code 1

Whenever food is placed in the mouth, taste receptors are stimulated. Simultaneously, different types of sensory fibre that monitor several food attributes such as texture, temperature, and odor are activated. Here, we evaluate taste and oral somatosensory peripheral transduction mechanisms as well as the multi-sensory integrative functions of the central pathways that support the complex sensations that we usually associate with gustation. On the basis of recent experimental data, we argue that these brain circuits make use of distributed ensemble codes that represent the sensory and post-ingestive properties of tastants.

The gustatory system enables animals to detect and discriminate among foods, to select nutritious diets, and to initiate, sustain and terminate ingestion for the purpose of maintaining energy balance. For most mammals, the decision to ingest a particular food depends not only on its taste but also on its appearance, familiarity, odor, texture, temperature and, importantly, its post-ingestive effects (for example, the ability to reduce hunger). For humans, such factors also include cultural acceptance as well as the social, emotional and cognitive contexts under which a given food is eaten. Previous reviews on gustatory processing tended to focus on either the molecular bases of peripheral transduction events or on central taste representations in isolation from other modalities. Here, we propose instead that the biological functions of gustation must be considered in combination with several sensory and physiological processes that occur simultaneously with taste receptor activation. According to this view, gustation is a distributed neural process by which information conveyed to the brain through specialized taste, orosensory and gastrointestinal fibers is integrated, so that the organism can engage in appropriate feeding behaviors. Such a view emerges from the analysis of recent experimental data showing that the neural mechanisms of gustation rely on neural ensemble codes supported by populations of neurons that are capable of encoding the multisensory properties of intra-oral stimuli under particular physiological states. Revealing the logic of the neural mechanism of gustation is currently a major topic in neurobiology, given the efforts made so far towards the understanding of how complex feeding behaviors can become dysfunctional (as in the case of obesity). We cover three main topics. First, we describe the interactions between various oral taste and somatosensory receptors in the PNS. We then focus on the convergence of gustatory, somatosensory and visceral influences at the brainstem level. Finally, we describe current data on the behavior of neural populations located in the forebrain relating to the multisensory and post-ingestive properties of intra-oral stimuli.

The peripheral gustatory system
Although the sense of taste is generally associated solely with the activation of taste buds, the act of placing food or drinks in the mouth automatically elicits responses from a different system that monitors the temperature and texture of the food. In this regard, gustation is inherently multisensory. It is generally accepted that there are five primary tastes: salt, sweet, bitter, umami (a savoury taste) and sour (acidic). However, every gourmet worth his/her salt is aware that this list should also include perceptual categories such as astringent, fatty, tartness, water, metallic, starchy, cooling, tingling and pungent. The subjective sensations associated with these non-primary tastes result from the co-activation of taste and specialized somatosensory neurons located in the oral cavity. These specialized neurons surround taste buds, and include different classes of mechano- and chemoreceptors
that transmit information on the food’s texture, weight and temperature to the brain mainly via the trigeminal system (FIG. 1).



The taste bud and associated neural afferents. In the oral chemosensory epithelia, onion-shaped structures known as taste buds contain 50–100 taste receptor cells (TRCs) of various types12. These TRCs are embedded in stratified epithelia and are distributed throughout the tongue, palate, epiglottis and oesophagus. On their apical end, taste cells make contact with the oral cavity through a small opening in the epithelium called the taste pore, which is filled with microvilli.

2




The plasma membranes of these microvilli contain many of the receptors responsible for detecting the presence of various tastants (FIG. 1). Tight junctions, located just below the microvilli, protect the basolateral side of the TRCs from potentially cell-damaging compounds that are placed in the mouth. Small clusters of TRCs are electrically and chemically coupled by gap junctions. As TRCs have resistances in the giga-ohm range, it has been suggested that the activation of any TRC in a cluster will affect the responses of others via gap junctions. On the palate and the anterior tongue, TRCs are innervated by the chorda tympani and greater superior petrosal branches of the facial nerve, respectively. These nerves transmit information about the identity and quantity of the chemical nature of the tastants. On the epiglottis, oesophagus and posterior tongue, TRCs are innervated by the lingual branch of the glossopharyngeal nerve and the superior laryngeal branch of the vagus nerve. These nerves are responsive to tastants and participate primarily in the brainstem-based arch reflexes that mediate swallowing (ingestion) and gagging (rejection). TRCs transmit information to the peripheral nerves by releasing ATP24 to P2X2/P2X3 purinergic receptors located on the postsynaptic membrane of primary afferents. Other transmitters such as serotonin, glutamate and acetylcholine might also be released.





Taste Bud Homeostasis in Health, Disease, and Aging 3
Taste receptor cells detect nutrients and toxins in the oral cavity and transmit the sensory information to gustatory nerve endings in the buds. Supporting cells may play a role in the clearance of excess neurotransmitters after their release from taste receptor cells. Basal cells are precursor cells that differentiate into mature taste cells. Similar to other epithelial cells, taste cells turn over continuously, with an average life span of about 8–12 days. To maintain structural homeostasis in taste buds, new cells are generated to replace dying cells. Several recent studies using genetic lineage tracing methods have identified populations of progenitor/stem cells for taste buds, although contributions of these progenitor/stem cell populations to taste bud homeostasis have yet to be fully determined. Some regulatory factors of taste cell differentiation and degeneration have been identified, but our understanding of these aspects of taste bud homoeostasis remains limited. Many patients with various diseases develop taste disorders, including taste loss and taste distortion. Decline in taste function also occurs during aging. Recent studies suggest that disruption or alteration of taste bud homeostasis may contribute to taste dysfunction associated with disease and aging.

Mechanisms for taste cell death
On average, 11% of taste cells are replaced daily in the adult mouse taste buds. It has been suggested that apoptosis is a major mechanism for cell death in taste buds. At any given time, in adult taste buds, the regulators for apoptosis, such as p53, Bax, and caspase-2, could be detected in 8–11% of cells. p53 and caspase-2 frequently colocalize with Bax in double-immunostaining experiments. In contrast, in postnatal day 7 mice, when most taste cells were young, no more than 1% of taste cells were positive for either p53 or Bax.

1. 9. http://www.nature.com.sci-hub.cc/nrn/journal/v7/n11/full/nrn2006.html
2. https://www.uni-mainz.de/FB/Medizin/Anatomie/workshop/EM/externes/Wartenberg/GKnospe3E.html
3. https://academic.oup.com/chemse/article/39/1/3/332985/Taste-Bud-Homeostasis-in-Health-Disease-and-Aging

Further readings :
Anatomy of the Tongue and Taste Buds
Molecular Mechanisms of Bitter and Sweet Taste Transduction*

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