Taste

TOPICS IN TASTE

Why taste? | What is flavour? | Anatomy and Physiology | Development of taste | Taste buds | Cells in taste bud | Taste transduction | Transmitter | Salt taste | Sour taste | Sweet taste | Bitter taste | Umami taste | Receptors | Modifying taste | Taste maps | Relay to the brain | Central pathways | Supertasters | Strange taste facts | Coca cola tastes great? | Smell and diet | Artificial sweeteners

Why taste?

Good food makes you happy for one thing - see the 50 Best Restaurants in the World. But, in addition, taste drives appetite and protects us from poisons. So, we like the taste of sugar because we have an absolute requirement for carbohydrates (sugars etc). We get cravings for salt because we must have sodium chloride (common salt) in our diet.

salt

sweet

Bitter and sour cause aversive, avoidance reactions because most poisons are bitter (most bitter substances are bad for you - certainly in excess) and off food goes sour (acidic). Why do medicines all taste bitter? Because they are, in fact, poisons and if you take too much they will harm you. We have an absolute need for protein, and amino acids are the building blocks for proteins, so the "new" taste quality umami (pronounced: oo-marmi) which is the meaty, savoury taste drives our appetite for amino acids. This taste has been known to the Japanese for a long time - but has only recently been recognised by the West. Bacon really hits our umami receptors because it is a rich source of amino acids. Recently, earlier in 2017, there have been papers suggesting that there are not just 5 tastes, but two more: fat and carbohydrate. However, a taste must have a specific mechanism (e.g. receptor) and be localised to the tongue, or at least the mouth, and send signals to the taste cortex of the brain. This is NOT true for fat and carbohydrate tastes so strictly speaking they cannot be considered as separate tastes. So, in my opinion, fat is not a separate taste. The fat "receptors" are CD36 receptors which are responsible for detecting fatty acids and these are found in many cells throughout the body.

What's the worst taste in the world? Apart from a "fatberg", Gizmodo has some suggestions - different people have different ideas (mine's vomit). Further to the "food makes you happy" 50 Best Restaurants theme (above) about 5 are in Spain which is where I live, so.....here I go, first stop "Tickets" restaurant in Barcelona!

Tickets restaurant Barcelona, one of World's top 50

Interesting fact: Cats don't taste sweet things, one of the two genes coding for the sweet receptor protein, Tas1r2, is defective.

So, when offered water or water sweetened with sugar they have no preference - cats are obligate carnivores, they must have meat. They are the only mammals to lack sweet taste.

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What is flavour? 

When most people talk about taste, they actually mean flavour (flavor US). Flavour is SMELL + TASTE, but mainly smell. Without smell food tastes really dull, so does drink. When we are hungry our appetite increases and our sense of smell becomes more acute, we smell things more intensely and this eases off once we've eaten. It is the flavour that makes food and drink so pleasurable. People who lose their sense of smell often have difficulty in controlling their weight either eating too much to compensate or not eating at all because they have lost the pleasure in food (and drink). Loss of taste or taste disturbances can have serious consequences and should be checked out - see MedicineNet.

Smell and diet

Scent-based weight-loss products deliver aromas that are supposed to reduce your appetite. One of the early scent-based products, the powdered food additive, Sensa, was withdrawn from the market after the Federal Trade Commission in the USA found that the product made false claims of effectiveness. A study by Alan Hirsch, M.D., who developed Sensa, is often cited as proof that aromatherapy aids weight loss. That study showed that volunteers who used an aroma inhaler lost an average of 2 percent of their body weight over six months. However, because the study lasted only six months, it didn't look at whether participants were able to maintain their weight loss over time. A few studies on the effects of odours on appetite have found that smelling sweet food odours, such as vanilla, banana and chocolate, tend to increase appetite, while neutral or non-food odours tend to decrease it. This suggests that the much publicised "vanilla patches" will not offer much assistance in weight loss.

Anatomy and Physiology of Gustation (taste)

In mammals, taste buds are groups of 30-100 individual elongated "neuroepithelial" cells (50-60 microns in height, 30-70 microns in width), which are often embedded in special structure in the surrounding epithelium, termed papillae (see Fig. 1 below). At the apex of the taste bud, microvillar processes protrude through a small opening, the taste pore, into the oral milieu. Just below the taste bud apex, taste cells are joined by tight junctional complexes that prevent gaps between cells. Food molecules cannot therefore squeeze between taste cells and get into the taste bud.

The development of taste

Newborns: indifferent or averse to salt
Babies: reject sour tastes, prefer sweet
6-24 months: develop preference for saline (salt solution)
3-24 month: babies reject MSG (monosodium glutamate) containing water but prefer sour with MSG added
Young children: A few young children go through a phase when they prefer very sour tastes, sour flavour is important to many cuisines the addition of a sodium salt to some, but not all, bitter tasting liquids enhances acceptance and reduces the perceived bitterness in 7- to 10-year-old children and their mothers
Children/adolescents: Prefer higher concentrations of sweet and salt than adults do not like bitter substances. Taste for bitter develops in adults with experience (trial and error)
26-75 years: thresholds for sucrose, salt, citric acid and quinine (bitter) increase - become less sensitive

Taste buds and taste papillae

Taste papillae can be seen on the tongue as little red dots, or raised bumps, particularly at the front of the tongue. These ones are actually called "fungiform" papillae, because they look like little button mushrooms. There are three other kinds of papillae, foliate, circumvallate and the non-gustatory filiform. Taste buds, on the other hand, are collections of cells on these papillae and cannot be seen by the naked eye. To illustrate the point, have a look at the diagram below. You can see that the taste buds are collections of cells situated on top of, or on the sides of, the different papillae.


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Figure 1 Distribution of taste papillae, types of papillae and a taste bud
Figure 1 shows the taste papillae on the tongue - 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. 

1. Fungiform papillae are located on the most anterior part of the tongue and generally contain one to several taste buds per papilla. They are innervated by the chorda tympani branch of the facial (Vllth cranial) nerve. They appear as red spots on the tongue - red because they are richly supplied with blood vessels. The total number of fungiform papillae per human tongue is around 200. Papillae at the front of the tongue have more taste buds (1-18) compared to the mid-region (1-9). It has been calculated that there are 1120 fungiform taste buds per tongue.
2. Foliate papillae are situated on the edge of the tongue slightly anterior of the circumvallate line. They are predominantly sensitive to sour tastes. Innervated by the glossopharyngeal (lXth cranial) nerve. On average 5.4 foliate papillae per side of the tongue, 117 taste buds per foliate papillae, total = 1280 foliate taste buds per tongue.
3. Circumvallate papillae are sunken papillae, with a trough separating them from surrounding wall. The taste buds are in tiers within the trough of the papillae. They are situated on the circumvallate line and confer a sour/bitter sensitivity to the posterior 2/3 of the tongue. Innervated by the glossopharyngeal (lXth cranial) nerve. 3-13 circumvallate papillae per tongue with 252 taste buds per papillae, total = 2200 circumvallate taste buds per tongue.
4. Filiform papillae are mechanical and non-gustatory. 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.

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Cells in taste bud (fig.1)

• Supporting cells - contain microvilli, appear to secrete substances into lumen of taste bud.
• Sensory receptor cell - has peg-like extensions projecting into lumen. These contain the sites of sensory transduction.
• Basal cells - these differentiate into new receptor cells. They are derived from surrounding epithelium. The cells are continuously renewed every 10 days or so.

Figure 2. A taste receptor cell
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Taste transduction

There are five basic tastes: salt, sour, sweet, bitter and umami. 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 (Chandrashekar et al, 2006 ). It has been shown 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 (Zhang et al., 2003). 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.

Salt taste

We have an absolute requirement for salt. It is an essential part of our diet (not too much though! 6 grams a day is the recommended amount - just over one teaspoon). Salt is sodium chloride (Na⁺Cl^-). Na⁺ ions enter the receptor cells via Na-channels. These are amiloride-sensitive Na⁺ channels (as distinguished from TTX-sensitive Na⁺
channels of nerve and muscle). The entry of Na⁺; causes a depolarization, Ca²⁺ enters through voltage-sensitive Ca²⁺ channels, transmitter release occurs and results in increased firing in the primary afferent nerve.

Sour taste

Sour is the taste of acid, eg citric acid (lemons). Acid is generally bad for you so this is a warning. Sticking your tongue across the terminals of a 9v battery activates sour receptors (I don't recommend it). Sour taste is acid and acid is protons (H⁺). There is exciting new evidence that there is an acid-sensing channel - the PKD2L1 channel (1).This channel is a member of the transient receptor potential channel (TRP) family and is a non-selective cation channel. The activity of PKD2L1 is gated by pH (H⁺ ion concentration). This new discovery displaces the previous ideas that H⁺ ions block K⁺ channels causing a depolarization, or that H⁺ ions enter the cell through ENaC channels. These mechanisms may exist but do not lead directly to sour perception.

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Sweet taste

There are receptors (T1R2 + T1R3) in the apical membrane that bind glucose (sucrose - a combination of glucose and fructose - and other carbohydrates). Binding to the receptor activates a G-protein which in turn activates phospholipase C (PLC-ß2). PLC generates IP3 and diacyl glycerol (DAG). These intracellular messengers, directly or indirectly, activate the TRPM5 channel and depolarization occurs. Ca²⁺ enters the cell through depolarization-activated Ca²⁺ channels, transmitter is released increasing firing in the primary afferent nerve.

Bitter Taste

Bitter substances bind to the T2R receptors activating the G-protein and causing activation of PLC. The second messengers DAG and IP3 are produced (by hydrolysis of phosphatidylinositol-4,5-bisphosphate) activating TRPM5 and mediating release of Ca2+ from internal stores. The elevated Ca2+ causes transmitter release and this increases the firing of the primary afferent nerve.

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Umami taste

Umami is the taste of certain amino acids (e.g. glutamate, aspartate and related compounds). It was first identified by Kikunae Ikeda at the Imperial University of Tokyo in 1909. It was originally shown (2,3) that the metabotropic glutamate receptor (mGluR4) mediated umami taste. Binding to the receptor activates a G-protein and this elevates intracellular Ca²⁺. More recently it has been found that the T1R1 + T1R3 receptors mediate umami taste (4) . Binding to the receptors activates the non-selective cation channel TRPM5 as for sweet and bitter receptors (i.e. via G-protein, PLC, IP3 and DAG - see above). Guanosine 5'-monophosphate (GMP) and inosine 5'-monophosphate (IMP) potentiate the effect of umami tastes by binding to another site of the T1R1 receptor.
Monosodium glutamate, added to many foods to enhance their taste (and the main ingredient of Soy sauce), stimulates the umami receptors. But, in addition, there are ionotropic glutamate receptors (linked to ion channels), i.e. the NMDA-receptor, on the tongue. When activated by these umami compounds or soy sauce, non-selective cation channels open, thereby depolarizing the cell. Calcium enters, causing transmitter release and increased firing in the primary afferent nerve.

1. The cells and logic for mammalian sour taste detection. Huang et al., (2006) Nature 442, 934-8.
2. Chaudhari et al, (1996) The taste of monosodium glutamate: membrane receptors in taste buds. J. Neurosci. 16, 3817-3826.
3. Kurihara & Kashiwayanagi (1998) Introductory remarks on umami taste. Annals NY Acad Sci 855, 393-397.
4. Nelson, G. et al (2002) An amino-acid taste receptor. Nature 416, 199-204.

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Monosodium gutamate

Monosodium glutamate is the main ingredient of Soy sauce. This is added to foods to enhance their flavour. As well as activating umami receptors, it probably works by activating NMDA receptors which are found in taste cells. NMDA receptors are integral receptor-ion channel complexes and when they open they allow an influx of Na⁺ and Ca²⁺ ions. This will depolarise the taste receptor cell and act as an excitatory influence. Then, far less of a particular taste will be required to cause the further depolarisation necessary to bring about transmitter ease.

Transmitter

Finger and colleagues (1) 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 fibres (2). Because the ATP is released via pannexin hemichannels rather than by vesicular fusion, Ca-influx is not necessary (3).

1. Finger et al., (2005) ATP signalling is crucial for communication from taste buds to gustatory nerves. Science 310, 1495-1499. 
2. Romanov, R.A. et al. (2007) Afferent transmission mediated by hemichanneks in mammalian taste cells. EMBO J 26(3), 657-667. 
3. Huang, Y.J. et al. (2007) The role of pannexin 1 hemihannels in ATP release and cell-cell communication in mouse taste buds. PNAS (USA) 104(15), 6431-6441.

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Receptors

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

Modifying taste

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.

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Miracle berries

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. You can buy miracle berry powder at the Miracle Fruit Shop. I have not tried miracle berries or the powder but know people who have and the effect is spooky - you can eat lemons and they taste sweet apparently.

Artificial sweeteners

Here is the structure of sucrose - our main sugar:

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 artificial sweeteners (e.g. saccharin) lead to the generation of IP3 and a rise in intracellular Ca2+ due to release from internal stores.
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Regional localisation of taste on the tongue (Taste maps)

Taste maps - wrong

There has been some controversy as to whether the familiar taste maps of the human tongue, which appear in every textbook, are correct. 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.
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Relay to the brain

Figure 3. Innervation of the tongue

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.

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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!

Central pathways

Primary gustatory fibres synapse centrally in the medulla (in a thin line of cells called the nucleus of the solitary tract). From there the information is relayed (1) to the somatosensory cortex for the conscious perception of taste and (2) to the hypothalamus, amygdala and insula, giving the so-called "affective" component of taste. This is responsible for the behavioural response, e.g. aversion, gastric secretion, feeding behaviour.

Supertasters

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.

Table 1

	% percent of population	*density of taste papillae cm-2
supertasters	25	165
normal  tasters	50	127
non-tasters	25	117

*at the tip of the tongue (from Yackinous and Guinard, 2002).

Strange taste facts

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).

Coca cola tastes great?

Until 1903, the world-famous soft drink contained a significant dose of cocaine. While the Coca-Cola Company officially denies the presence of cocaine in any of its products — past or present — historical evidence suggests that the original Coca-Cola did, in fact, contain cocaine. While the modern-day recipe for Coca-Cola is a highly prized company secret, there is reason to believe that the beverage still contains the same non-narcotic coca-leaf extract that it did in 1929. According to The New York Times, the Coca-Cola Company was continuing to import coca leaves from Peru and Bolivia until at least the late 1980s (read more in Live Science and Scientific American).

Durian fruit

The smelly durian fruit

The durian fruit smells horrible. Some people cannot bear to eat it because it smells so foul. But it is called the "King of Fruits" and tastes delicious. It is very large (can be the size of a football) and comes from South East Asia. In Singapore you can get fined $1000 SGD for taking it on public transport.

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Bibliography

1. Signals and Perception edited by David Roberts (2002). Open University - Palgrave Macmillan.
2. The Senses by Barlow by H.B and Mollon, J.D. (1982). Cambridge University Press.
3. Handbook of olfaction and gustation by Doty, R.L. (1995). Marcel Dekker.
4. The Chemical Senses by Moncrieff, J.W. (1967), pp 108-112.
5. Neurophysiology by Carpenter, R.H.S. (1995), 3rd edition.