INDEX (click on topic):
A tutorial on
the sense of taste
Compiled by Tim Jacob
Cardiff University, UK
|Anatomy||Nerves in Tongue||Salt Taste||Sweeteners||Transduction|
|Bitter||Modifying Taste||SMELL||Taste buds||Umami||Strange facts|
|Cells||Papillae||Sour||Taste Maps||Why Taste?||Links|
|Fat taste||Physiology||Sweet||Taste Transmitter||Bibliography|
News and current debates
Is obesity genetic? Largest ever genome-wide study published in the journal Nature (Feb 11, 2015; DOI:10.1038/nature14177 & DOI:10.1038/nature14132) strengthens genetic link to obesity (Daily Mail comment). Scientists found 97 'obesity genes' that seem to work by changing how the brain regulates appetite. These genes can explain why some people can't resist eating - and are more likely to pile on the pounds. “Our work clearly shows that predisposition to obesity and high BMI is not due to a single gene or genetic change,” says Elizabeth Speliotes, senior author of the study at the University of Michigan Health System. “The large number of genes makes it less likely that one weight loss solution will work for everyone and opens the door to possible ways we could use genetic clues to help defeat obesity.”
However, another study published at more or less the same time by Joan Costa-Font, Mireia Jofre-Bonet Julian Le Grand, based at the Centre for Economic Performance, London School of Economics and Political Science (LSE) concludes differently “It's the lifestyle of parents - rather than their genes - that is mainly responsible for children being overweight”.
Artificial sweeteners linked to obesity epidemic
More on obesity and sweeteners
The tastey part of meat is the fat (all sorts of interesting tastes dissolve in fat) and this fat coats the taste papillae (which contain the taste buds) as you chew. This reduces their sensitivity, so the next mouthful isn't as tastey. The tannin in the red wine acts to remove this fat (tannin is a surfactant). White wines go poorly with meat because they don't contain tannins (Ronald Lorenzo, Chemistry in Use, chap 14, p542).
FUNCTION of TASTE
Go to topFigure 1.Papillae and taste buds (often mixed up - papillae are visible with the naked eye, taste buds are not)
Figure 1 shows the taste papillae (on the left) - there are fungiform, foliate and circumvallate papillae. Taste buds are situated on the taste papillae (middle section). At the base of the taste bud, afferent taste nerve axons invade the bud and ramify extensively, each fibre typically synapsing with multiple receptor cells within the taste bud .
In mammals taste buds are located throughout the oral cavity, in the pharynx, the laryngeal epiglottis and at the entrance of the eosophagus. Taste buds on the dorsal lingual epithelium are the most numerous (total number of taste buds, all classes, = 4600 per tongue) and best-studied taste end-organs. Here, taste buds are contained within four major classes of papillae.
In addition there are 2500 taste buds on the epiglottis, soft palate, laryngeal and oral pharynx. Many of these taste buds are innervated by the facial nerve (Vllth cranial nerve).
The number of taste buds declines with age.
There are five basic tastes: salt, sour, sweet, bitter and umami.
The current thinking1 is that sweet, amino acid (umami), and bitter taste converge on a common transduction channel, the transient receptor potential channel TRPM5, via phospholipase C (PLC) (see Figure 2). TRPM5 is a newly discovered TRP related to other channels in sensory signalling systems.
It has been shown2 that PLC, a major signaling effector of G-protein coupled receptors (GPCRs), and TRPM5 are co-expressed with T1Rs and T2Rs and are vital for sweet, amino acid, and bitter taste transduction. Activation of T1R or T2R receptors by their respective tast molecules would stimulate G proteins, and in turn PLC (PLC-ß2). The activation of PLC generates two intracellular messengers - IP3 and diacylglycerol (DAG) - from the hydrolysis of phosphatidylinositol-4,5-bisphosphate (PIP2) and opens the TRPM5 channel, resulting in the generation of a depolarizing receptor potential. Other additional pathways may modulate sweet, amino acid, or bitter taste reception but would not, themselves, trigger a taste response. It is not at present known how PLC activates TRPM5 or whether DAG is involved. Future experiments should help reveal the G proteins for the various taste modalities and the mechanism of TRPM5 gating.
It is suggested that the TRPM5 channels are calcium sensitive, thus IP3 would activate the TRPM5 channels by releasing Ca2+ from internal stores - depolarization would follow and this would release the transmitter (ATP - see "Transmitter" below) an increase the firing rate of the gustatory nerve..
cells and logic for mammalian sour taste detection. Huang et al., (2006)
Nature 442, 934-8.
Finger and colleagues1 showed that all sweet, bitter, sour, salty and umami nerve responses were lost in the purinergic double-knockout mouse. This suggests that ATP (a purinergic agonist) is the taste neurtransmitter, released by the receptor cells to activate the primary afferent nerve. The taste receptor cells release ATP in a non-vesicular fashion to activate the gustatory nerve fibres2. Because the ATP is released via pannexin hemichannels rather than by vesicular fusion, Ca-influx is not necessary3.
Sweet, bitter and sour taste receptors have recently been cloned. A summary of the different types of receptor responsible for each of the 5 taste modalities is given below.
Go to top
Bitter receptor family - T2Rs
Sweet and umami receptors
Liao, J.; Schultz, P. G. Three sweet receptor
genes are clustered in human chromosome 1. Mammalian Genome 14: 291-301,
Sour is the taste of acid, i.e. protons (H+).
In August 2006, Huang et al4 published a paper showing that mice in which cells expressing PKD2L1 (polycycstic kidney disease-like channel) were ablated (knocked out) were completely unable to detect sour substances. PKD2L1 is a member of the TRP (transient receptor potential) superfamily of ion channels. They are non-selective cation channels. PKD2L1 is gated by pH (H+ ion concentration), a decrease in pH (acidity) openingthe channel and causing a depolarizing receptor potential. This activates voltage-dependent Ca2+ channels, evelating intracellular Ca2+ . This in turn causes the release of transmitter (now thought to be ATP).
References for taste receptors
Have a look at the structure of sweeteners - most sweeteners have a structure very different from that of sweet tasting compounds, e.g. glucose.
Saccharin - Discovered in 1879 when a Johns Hopkins worker inadverently licked his fingers. Saccharin is only sweet to humans. Bees/butterflies which normally crave the sweetness of nectar, do not treat it as a desirable substance.
Cyclamate - Discovered by accident. A graduate student at the University of Illinois in 1937 was smoking a cigarette that came into contact with some.
Aspartame - James Schlatter licked fingers in preparing to pick up a peice of weighing paper. It is a combination of two naturally occurring amino acids (aspartic and phenylalanine). Alitame, similar to aspartame in that it combines two amino acids (alanin and aspartic acid) into a dipeptide, is about 2,000-times sweeter than sugar.
Sucralose - A chloride-containing carbohydrate product some 600-times sweeter than sugar. Discovered when a foreign student (Shashikant Phadnis) working in Prof Leslie Hough's lab at King's College, London, misunderstood a request for "testing" as "tasting".
Some plant proteins, e.g. Monellin and Thaumatin, taste 10,000 times as sweet as sucrose (a disaccharide made up of a glucose and a fructose molecule). Salts of lead and beryllium also taste sweet.
Certain artifical sweeteners (e.g. saccharin) lead to the generation of IP3 and a rise in intracellular Ca2+ due to release from internal stores.
Taste exhibits almost complete adaptation to a stimulus - perception of a substance fades to almost nothing in seconds. Taste can be suppressed by local anaesthetics applied to the tongue. Amiloride, a blocker of epithelial Na channels, reduces salt taste in humans and adenosine monophosphate (AMP) may block the bitterness of several bitter tasting agents. Naturally occuring compounds include, gymnemic acid (a product of the Indian tree/shrub Gymnema sylvestre) decreases the sweet perception by competitive inhibition of the sweet receptor. Artichokes have the opposite effect, enhancing sweet taste (the active compounds in this case are chlorogenic acid and cynarin) by suppression of sour and bitter taste receptors. Miracle fruit turns sour tastes sweet. The active ingredient, "miraculin", binds to a site near the sweet receptor. When sour substances then are tasted, a conformational change in the taste cell membrane occurs in such a way as to bring the miraculin molecule into contact with the sweet receptor, activating it.
Taste maps are wrong!The taste map of areas of different tast sensitivity on the tongue has been dismissed as flawed. For some time there has been some controversy as to whether the familiar taste maps of the human tongue, which appear in every textbook (and certain websites on taste, mentioning no names!), are correct - they are not (see review by Chaudhari & Roper, Journal of Cell Biology 190; 285-296, 2010). Taste sensation can be localised on the tongue but does the tongue have regions that are more sensitive to one taste modality than another? Fungiform papillae are concentrated on the anterior tip of the tongue and anterior lateral margins in humans and it has been demonstrated that NaCl threshold was inversely related to the number of fungiform papillae (more papillae = more sensitivity, lower threshold). In a study of human fungiform papillae it was found that taste buds can respond to NaCl only or to both NaCl and sucrose. The responses to NaCl and sucrose occurred in different cells within the taste bud. Thus, one can infer that fungiform papillae are salt-sensitive but this does not mean they are insensitive to other tastes. Bitter receptors are not uniformly distributed over the tongue. In rats the bitter receptors are expressed in a subset of taste cells in all papillae but they are more concentrated in foliate and circumvallate papillae situated at the sides and the back of the tongue. Furthermore, alpha-gustducin, which is the G-protein coupled to the T2R bitter receptors (see below), is expressed more in circumvallate than fungiform papillae in the rat. One rather more empirical approach to resolving this question is to stimulate the different areas of the tongue directly. Thermal stimulation of the anterior sides of the tongue in humans (fungiform papillae and the chorda tympani nerve) evokes sweet and salt/sour taste. While thermal stimulation of the rear of the tongue (foliate/circumvallate papillae and glossopharyngeal nerve) causes a different relationship between temperature and taste to the anterior stimulation. One can conclude that the classical "taste map" is an over simplification. Sensitivity to all tastes is distributed across the whole tongue and indeed to other regions of the mouth where there are taste buds (epiglottis, soft palate), but some areas are indeed more responsive to certain tastes than others.
Taste receptor cells do not have an axon. Information is relayed onto terminals of sensory fibres by transmitter. These fibres arise from the ganglion cells of the cranial nerves Vll (facial - a branch called the chorda tympani) and lX (glossopharyngeal) (see Figure 3).The first recordings from sensory fibres showed an optimal response to one stimuli, but a smaller response to other taste stimuli.
There was been much evidence that taste is determined by the pattern of active (firing) fibres, i.e. by "across-fibre pattern" rather than "labelled-line". However, the molecular biologists have provided some fairly convincing evidence that taste operates by the "labelled-line" mechanism - knocking out specific taste receptor genes rendered mice completely insensitive to that taste modality - can't argue with that! But, the fact remains that many phenomena can only be explained by cross fibre patterns of activity. The pedulum swings between these two theories - the answer (?) - probably lies in-between!
It has been found that some people have more than the normal number of taste papillae (and taste buds). They are distinguished by their increased density of fungiform papillae and their exterme sensitivity to the chemical n-propylthiouracil (PROP). Supertasters - 25% of the population (and more women than men) - tend not to like green vegetables and fatty foods. This has a genetic origin and the gene responsible is TAS2R38 - there are a number of DNA variations (called polymorphisms) of this gene. One variant (PAV) confers sensitivity to PROP and the other (AVI) confers insensitivity to PROP - heterozygotes, i.e. those who have one of each, have an intermediate sensitivity. The gene seems to be responsible for the number of fungiform papillae. Supertasters have many more fungiform papillae and therefore more taste buds.
There appears to be a correlation between TAS2R38 and alcoholism1, with the AVI variants having an increased intake of alcohol. Those who find PROP very bitter also find alcohol less pleasant.
* at the tip of the tongue (from Yackinous & Guinard, Appetite (2000) 38, 201-209).
Taste is mainly smell. Hold your nose, close your eyes, and try to tell the difference between coffee or tea, red or white wine, brandy or whisky. In fact, with blocked nose (clothes peg or similar) you can't tell the difference between grated apple and grated onion - try it! Of course, this is because what we often call taste is in fact flavour. Flavour is a combination of taste, smell, texture (touch sensation) and other physical features (eg. temperature).
Asparagus makes your pee smell. This can happen very quickly after eating asparagus but not with everyone. You need a special enzyme to produce the smelly mercaptan that causes the effect - not everyone has it and, to confuse matters further - not everyone can smell the odour produced.
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