Taste - AccessScience from McGraw-Hill Education http://www.accessscience.com/content/taste/678600

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Article by:

Pfaffmann, Carl Department of Psychology, Rockefeller University, New York, New York.

Chaudhari, Nirupa Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, Florida.

Roper, Stephen D. Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, Florida.

Publication year: 2014

DOI: http://dx.doi.org/10.1036/1097-8542.678600 (http://dx.doi.org/10.1036/1097-8542.678600)

Content

Anatomy

Qualities

Sensitivity

Sour

Salt

Sweet

Bitter

Umami

Adaptation

Nutrition and taste

Bibliography

Additional Readings

Taste, or gustation, is one of the senses used to detect the chemical makeup of ingested food—that is, to establish its

palatability and nutritional composition. Flavor is a complex amalgam of taste, olfaction, and other sensations, including those

generated by mechanoreceptor a nd thermoreceptor sensory cells in the oral cavity. Olfactory (smell) sensory cells of the nose

are particularly important in the perception of flavor. Taste sensory cells respond principally to the water-soluble chemical

stimuli present in food, whereas olfactory sensory cells respond to volatile (airborne) compounds. See also: Sensation

(/content/sensation/614600)

Anatomy

The sensory organs of gustation are termed taste buds. In humans and most other mammals, taste buds are located on the

tongue in the fungiform, foliate, and circumvallate papillae and in adjacent structures of the throat. There are approximately

5000 taste buds in humans, although this number varies tremendously from person to person. Taste buds are goblet-shaped

clusters of 50 to 100 long slender cells. Microvilli protrude from the apical (upper) end of sensory cells into shallow taste

pores. Taste pores open onto the tongue surface and provide access to the sensory cells. Taste cells are modified epithelial

cells that develop at the base of the taste bud, differentiate into functional sensory cells, and ultimately die. This cycle of

differentiation, decline, and replacement, which lasts from 8 to 10 days, continues as long as the nerve supply to the taste

buds remains intact. When the taste nerves are cut, taste buds disappear. Taste buds reappear when the peripheral taste

nerve fibers regenerate and reinnervate the tongue epithelium. Individual sensory nerve fibers branch profusely within taste

buds and make contacts (synapses) with taste bud sensory cells. Taste buds also contain supporting and developing taste

cells (Fig. 1). See also: Tongue (/content/tongue/700200)

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Fig. 1 Drawing of an electron microscopic section through a rabbit taste bud. A taste receptor cell (no. 3) is shown making two synaptic contacts w ith sensory nerve fi bers. Several cells (no. 2) that make numerous physical contacts with nerve fibers also may be involved in impulse transmission. D arker cells (no. 1) are presumed to be supporting cells. ( After R. G. Murray, The ultrastructure of taste buds, in I. Friedmann, ed., The Ultrastructure of Sensory Organs, pp. 3–81, 1973)

The anterior two-thirds of the tongue is innervated by a sensory branch of the facial nerve (cranial nerve VII), the posterior

tongue by the glossopharyngeal nerve (cranial nerve IX), and the throat and larynx by branches of the vagus nerve (cranial

nerve X). These nerves carry information from touch, temperature, and pain sensory cells, as well as from taste buds. The

taste fibers from the anterior part of the tongue branch from the lingual nerve in a smaller nerve called the chorda tympani

(sensory branch of the facial nerve). The chorda tympani nerve traverses the eardrum en route to the br ainstem. When the

chorda tympani is damaged, as in the surgical removal of the tympanum, taste sensitivity is lost on the anterior two-thirds of

the tongue on the same side as the surgery because the nerve is interrupted.

The cell bodies (somata) of taste nerve fibers (primary sensory afferent fibers) are clustered in several small ganglia nestled

within the cranium but outside the brain itself. In the brain, taste fibers from the lingual, glossopharyngeal, and vagus nerves

converge in the solitary tract and its nucleus in the medulla oblongata. These fibers terminate on neurons in a region

contiguous to the area where touch and temperature sensory nerve fiber s from the tongue also en d. Second-order fibers from

these neurons ascend to a cluster of small neurons located in the ve ntrobasal thalamus. (In rodents, another relay site—the

pontine taste nucleus, or parabrachial nucleus—is interposed between the nucleus of the solitary tract and the thalamus; Fig.

2.) From the thalamus, neurons project to the lateral sensory cortex to two areas, one a mixed tactile-taste zone and the other

largely a taste area, the primary gustatory cortex. This thalamocortical system is concerned largely with discrimination among

different tastes. Outputs from the primary gustatory cortex terminate in the orbitofrontal cortex, where axons from the olfactory

sensory cortex and other sensory cortical areas converge. This area of the brain appears to be dedicated to processing more

complex perceptions such as flavor, where information from several sensory modalities is integrated. A second projection

from the pontine taste area travels more ventrally, sending collaterals to the hypothalamus and other limbic structures to

terminate ultimately in the central nucleus of the amygdala. This ventral pathway is presumed to mediate taste preferences,

aversions, and hedonic responses (pleasantness or un pleasantness) of taste (Fig. 2). See also: Brain (/content/brain

/093200); Nervous system (vertebrate) (/content/nervous-system-vertebrate/449300)

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Fig. 2 Schematic drawing of the two neural pathways for taste in the rodent brain. (After R. Norgren, Taste pathways to hypothalamus and amygdala, J. Comp. Neurol., 166:17–30, 1976)

Qualities

The basic taste qualities experienced by humans include sweet, salty, sour, and bitter. (In some species, pure water also

strongly stimulates taste bud cells.) A fifth taste, umami, is now recognized by many as distinct from the other qualities.

Umami is a Japanese term roughly translated as “good taste” and is approximated by the English term “savory.” It refers to

the taste of certain amino acids such as glutamate (as in monosodium glutamate) and certain monophosphate nucleotides.

These compounds occur naturally in protein-rich foods, including meat, fish, cheese, and certain vegetables.

The middorsum (middle top portion) of the tongue surface is insensitive to all tastes. Only small differences, if any, exist for

the taste qualities between different parts of the tongue (contrary to the “tong ue maps” of taste sensitivities that are commonly

published). Electrophysiological records from individual taste bud sensory cells show increased depolarization with an

increased concentration of an effective stimulus. This leads to the release of neurotransmitters at synapses on the afferent

taste nerves (Fig. 1) and an increase in frequency of nerve impulses therein (Fig. 3). No simple direct relationship exists

between chemical stimuli and a particular taste quality except, perhaps, for sourness (acidity). Sourness is due to H + ions.

The taste qualities of inorganic salts are complex, and sweet and bitter tastes are elicited by a wide variety of diverse

chemicals.

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Fig. 3 Typical oscillographic record of impulses in a single taste sensory nerve fiber of a rat. (After C. Pfaffmann, Gustatory nerve impulses in rat, cat and rabbit, J. Neurophysiol., 18:432–433, 1955)

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Sensitivity

Specific sensitivity to particular chemicals is attributed to ion channels and to molecular receptors on the surface of sensory

cells in taste buds, particularly on the apical membrane. Taste bud sensory cells are believed to have a spectrum of chemical

sensitivities that differs from cell to cell. Some taste bud sensory cells probably respond to only one of the basic taste

qualities, whereas others may be less discriminating and respond to multiple chemicals. This suggests that taste bud sensory

cells possess more than one type of molecular receptor o n their membranes. Alternatively, the surface membrane receptors

themselves may be somewhat broadly sensitive to chemical stimuli. The sensitivity of individual taste bud sensory cells and

their taste re ceptors is currently a topic of intense investigation.

More is known about the chemical sensitivity of sensory nerve fibers that innervate taste buds (chorda tympani,

glossopharyngeal, and vagal). These fibers represent the sensory information output from taste buds. A fraction of the fibers

are activated when the tongu e is stimulated with a specific chemical or closely related compounds such as sucrose and

fructose, and thus are narrowly receptive to chemical stimulation. However, even fibers with a broad sensitivity to diverse

chemicals usually respond best (that is, give the highest frequency of action potentials) to a single type of chemical stimulus.

The perception of taste quality (sweet, sour, salty, bitter, umami) is probably coded by the concurrent activation of some

sensory fibers that are highly selective for certain chemical compounds as well as by other fibers that are less selective. That

is, the pattern of activity within a heterogeneous population of sensory nerve fibers elicited by a particular taste stimulus

determines taste perception (Fig. 4). No single homogeneous population of nerve fibers carries the information for a given

taste quality. Various statistical procedures (such as factor analysis and multidimensional scaling) have been used to analyze

these patterns of activity in taste fibers and have provided quantitative evidence for the existence of sweet, sour, salty, bitter,

and umami taste qualities. See also: Chemoreception (/content/chemoreception/128600)

Fig. 4 Bar diagram of the different sensitivity patterns in (a–i) each of nine single sensory fibers from a rat. Dark color indicates number of impulses during first second of discharge to each of five test solutions shown along base: HCl (hydrochloric acid); KCl (potassium chloride); NaCl (sodium chloride); Qu (quinine); Suc (sucrose). Light color on fiber e shows relative amount of neural activity in total nerve (sum of all fibers) to same test solutions. (After C. Pfaffmann, Gustatory nerve impulses in rat, cat and rabbit, J. Neurophysiol., 18:432–433, 1955)

Sour

Studies by different investigators of human sour taste (acidity) reveal a wide range of thresholds for detection. For instance,

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hydrochloric acid (HCl) can be tasted at a concentration of about 0.0005 molar (M). Sourness increases with increases in

hydrogen ion concentration, but weak organic acids are more sour than would be predicted from their hydrogen ion

concentration. Increasing carbon chain length in the aliphatic acid series, for example, appears to e nhance the potency of

taste stimulation.

A number of explanations for how acid-sensitive taste sensory cells respond to hydrogen ions have b een put forth. Possible

mechanisms include the following:

1.

Penetration of positively charged hydrogen ions (protons, H +) through specific ion channels such as epithelial sodium

channels (ENaC) in the apical membrane. The influx of H+ would de polarize an d excite the ta ste sensory cell. Taste b ud

sensory cells express ENaC channels, and pharmacological agents that block these channels reduce sour sensitivity in

certain species, including humans.

2. Activation of cation-selective ion channel receptors by protons. Mammalian degenerin-1 (MDEG1) is one such receptor that

has been identified in taste bud sensory cells in mice. Activation of MDEG1 by H + would allow the influx of cations such as

sodium (Na +), again depolarizing and exciting the taste sensory cell.

3. Block of potassium-selective ion channels in the apical membrane by H +. Potassium ions (K +) tend to leave the cell through

these channels, keeping the sensory cell at a negative resting potential. Any agents, such as protons, that block these

channels will result in depolarization and excitement of the taste sensory cell, as has been demonstrated in amphibian taste

bud sensory cells.

4. Possible stimulation of specialized ion channels called hyperpolarization-activated, cyclic-nucleotide-gated (HCN) or

pacemaker channels by H +. Such channels have been identified in taste bud cells in some species. Their stimulation would

lead to depolarization of the cell.

Perhaps some combination of all the above events underlies sourness, and sour tast e mechanisms may differ from sp ecies to

species. The final answer is not yet achieved. See also: Biopotentials and ionic currents (/content/biopotentials-

and-ionic-currents/083900)

Salt

Most salts, including sodium chloride (NaCl), elicit other qualities, such as bitter or sour, in addition to salty. The dominant

taste elicited by table salt is salty. Low-molecular-weight salts are predominantly salty, many higher-molecular-weight salts

are bitter, and the salts of lead and beryllium are sweet. The median human threshold for detecting sodium chloride is

approximately 0.01 M, but a wide range of values has been reported. Both the an ion (for example, Cl −) an d cation (for

example, Na +) contribute to saltiness and to stimulus potency. According to one theory, salt-sensitive taste bud cells are

stimulated by the influx of Na+ through ENaC channels in their cell membrane. ENaC channels are found in other tissues in

the body that are involved in Na+ transport, such as renal tubules. Blocking ENaC channels with pharmacologic agents has

been reported to reduce salt taste responses in some species. (However, the effects of blocking ENaC channels on hu man

salt taste are controversial at present.) Further, H+ also passes through ENaC channels, and agents that block ENaC

channels alter sour taste. These observations raise the conundrum that the same mechanism (ENaC channels) appears to

underlie both salt and sour tastes. However, there is no complete e xplanation yet for these observations. See also: Salt

(food) (/content/salt-food/599500)

Sweet

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Sweet taste is associated largely with organic compounds such as sugars, alcohols, glycols, and sugar derivatives, with the

exception of certain lead and beryllium salts. Sucrose thresholds for humans have a median value of 0.1 M, whereas the

synthetic sweetener saccharin is 700 times more potent. The discovery that L-aspartyl-L-phenylalanine methyl ester

(aspartame) is extremely sweet has led to further study of other dipeptides, but not all are sweet; some are sour, bitter,

umami, or even tasteless. Some proteins have been discovered that elicit sweet taste with thresholds for humans in the 10 −7

M concentration range. Slight changes in spatial arrangement render a sweet molecule tasteless or even bitter (Fig. 5). See

also: Aspartame (/content/aspartame/055050)

Fig. 5 Taste quality changes when spatial arrangements within the molecule change. (After S. S. Stevens, ed., Handbook of Experimental Psychology, Wiley, 1951)

Studies of t he specific blockage of s weet sensitivity by gymnemic acid, which does not affect salt, sour, or bitter, point to the

existence of specific sweet receptors on the surface of taste bu d sensory cells. One theory attributes the sweet taste to

substances with a molecular system AH-B, where A and B are electronegative atoms separated by a distance of 0.3

nanometer. The AH moiety is a proton donor and the B moiety a proton acceptor. Sweet taste receptors are assumed to

possess a complementary AH-B system with which the stimulus system can interact, forming two intersystem hydrogen

bonds. More recent formulations add a third molecular feature. Two candidate receptors for sweet taste have recently been

cloned from human and rodent taste buds. These receptors (T3Rs) are G protein–coupled receptors, meaning that

stimulation of the sweet receptor activates a cascade of intracellular enzymatic reactions involving G proteins. One such G

protein that is associated with sweet taste is gustducin, which is found in taste bud cells and in some related cells. The net

result of activating the sweet receptors on sweet-sensitive taste bud cells appears to be the block of K + channels, which

depolarizes and excites taste bud sensory cells.

Bitter

Bitter is elicited by many chemical compounds and may be found in association with sweet and other taste qualities. An

increase in the molecular weight of inorganic salts or in the length of a carbon chain of organic molecules may be associated

with increased bitterness. Typical of substances with the bitter taste are the alkaloids such as quinine, caffeine, and

strychnine, which are often toxic. A median threshold value for q uinine h as been cited at 0.000008 M. Taste blindness is an

inherited inability to taste the bitterness of specific compounds such as phenyl thiocarbamide (PTC) and substances with the

thiocarbamide group (N C S). About one-third of Caucasians are nontasters of PTC.

Two mechanisms have been proposed to explain how bitter-sensitive taste bud cells respond to stimulation. For example,

certain bitter compounds directly block K + channels, a mechanism shared by sour and sweet sensing cells, and bitter taste

receptors have been cloned and identified in human and rodent taste bud cells. Bitter taste receptors (T2Rs), like the

candidate sweet taste receptors (T3Rs), are also G protein–coupled receptors. Unlike the candidate sweet receptors that

have be en identified to da te, a large family of genes (about 30) encode bitter taste receptors. The G protein gustducin is also

believed to interact with bitter receptors and activate an intracellular signaling cascade. Mice lacking gustducin show reduced

taste responses to sweet and bitter chemicals. Thus, the determining factor for whether a given taste bud sensory cell

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responds to bitter or sweet is which receptor or receptors are expressed on the apical surface.

Umami

Umami, or savory taste, is stimulated by L-glutamate and certain nucleotide monophosphates such as 5′-inosine

monophosphate and 5′-guanosine monophosphate. The threshold for human perception of L-glutamate is about 0.0008 M.

Humans and other mammals find L-glutamate a preferred taste. Consequently, the natural glutamate content of prepared

foods is often increased to enhance palatability by adding glutamate in the form of monosodium glutamate (MSG) or as

protein hydrolysates. An important characteristic of umami is the synergistic interaction between glutamate and nucleotide

monophosphates. Low concentrations of glutamate and n ucleotide monophosphates interact to generate a robust savory

taste.

A candidate G protein–coupled receptor for umami has been identified. It has been termed taste-mGluR4 and is a variant of

the synaptic glutamate receptor mGluR4. The G proteins and enzymes stimulated by taste-mGluR4 have not yet been

identified.

Adaptation

Prolonged exposure of the tongue to a taste stimulus decreases the response to that stimulus. This phenomenon, seen as a

decrease in nerve activity or in the perceived intensity of the stimulus, is called adaptation. Adaptation b y flowing taste

solutions continuously over the tongue may lead to a rise in threshold or even complete disappearance of the particular taste

sensation. Not only does that taste sensation disappear, but water and all concentrations of the stimulus at or below that used

for adaptation show a contrasting taste that is often quite intense. Sodium chloride and sucrose adaptation tends to produce a

bitter subadapting taste; adaptation to HCl and quinine produces a sweet subadapting taste. A salty taste is less common but

may follow adaptation to compound sour-bittersweet substances such as urea. That bitter or sour taste can be masked by

sweetening agents is well attested by the use of sweetners in coffee or in sour lemonade.

Nutrition and taste

The ability of an organism to select nutritious or necessary ingredients of the diet by taste can be demonstrated with the

self-selection technique, in which an animal is given free choice among individual containers with necessary nutrients in pure

form. After certain physiological stresses, like glandular imbalances, the selection of the various nutritive agents often shows

compensatory changes. A severely salt-deficient rat (adrenalectomized) may show a significant increase in the intake of

sodium chloride sufficient to counteract the usually fatal outcome in the absence of salt replacement therapy. Similar ef fects

have been noted in children; but in adults, food habits, cultural conditioning, learning, and other complex psychological factors

play significant enough roles in food acceptance to override the physiological factors controlling behavior. Nonetheless, food

palatability, as determined by taste, olfaction, and other sensory effects, has such a profound effect on food acceptance that a

substantial applied science of flavor technology has developed. See also: Chemical senses (/content/chemical-senses

/127700)

Carl Pfaffmann

Nirupa Chaudhari

Stephen Roper

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Molecular Approach, 3d ed., Academic Press, San Diego, 2001

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Additional Readings

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N. V. Kulkarni, Clinical Anatomy: (A Problem Solving Approach), 2d ed., Jaypee Brothers Medical Publishers, New Delhi,

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X. Li, G. Servant, and C. Tachdjian, The discovery and mechanism of sweet taste enhancers, Biomol. Concepts,

2(4):327–332, 2011 DOI: 10.1515/bmc.2011.021 (http://dx.doi.org/10.1515/bmc.2011.021)

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