Neural Basis Of Taste Research Paper

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The sense of taste is located at the interface between the uncontrolled chemical environment beyond the body and the highly regulated biochemical environment within. It serves to select, from among a vast array of candidates, those chemicals that satisfy the biochemical needs while identifying for rejection those that have proven toxic. This is accomplished through transduction mechanisms at the receptor level that permit the recognition of sugars, salts, acids, alkaloids, amino acids, fats, and starches. Peripheral taste nerves carry the signal to the brain stem where it activates reflexes for swallowing nutrients or rejecting toxins, then on to the cortex for recognition, and to the lower forebrain for an analysis of pleasure or disgust.

1. Sensitivity To Chemicals

The skin is only a crude chemical detector of deviations from pH 7 or certain plant irritants. The exceptions to this insensitivity occur at the points where chemicals enter the body: the nose and mouth. Here, chemical sensitivity is refined, complex, and subtle, for decisions must be made about which substances to admit. Taste may be viewed as the beginning of a long chemosensory tube that extends through the intestines, with receptors along its length that are sensitive to the products released by digestion. Thus, taste should be, and is influenced by the visceral signals that are a continuation of its own function. Together, taste and visceral sensations represent a core of chemical sensitivity that permits an animal to detect a subset of nutrients from an array of toxic or useless chemicals that surround them. What distinguishes taste is not that it recognizes chemicals—glucose is detected in the pancreas, sodium in the kidneys, and amino acids in the duodenum by similar mechanisms to those in the mouth—but that it does so before the irrevocable decision to swallow has been made. While preliminary assessments are made by other senses, notably vision and smell, and through familiarity and cultural norms, nonetheless, taste is the final arbiter of what is taken into the body. Every chemical that enters the mouth goes on trial, and the only verdicts are swallow or not swallow.

2. Taste Projections Into The Nervous System

Taste input is carried through peripheral nerves to the hindbrain of the central nervous system, from which it projects to at least four locations to mediate distinct functions.

2.1 Somatic Reflexes To Swallow Or Reject

Clusters of taste cells in the brain stem send projections to local motor nuclei that coordinate acceptance– rejection reflexes. These are based on a preliminary analysis of the chemical composition of a potential food, and elicit swallowing if the substance is deemed nutritious or rejection if it is toxic. The reflexes are fully integrated in the brain stem and are stereotypical for each basic taste. Consequently, they are not altered even by the loss of all neural tissue above the level of the midbrain (Grill and Norgren 1978). This chemical monitor is intact in humans by the seventh gestational month (Steiner 1979).

2.2 Visceral Reflexes To Aid Digestion

A second set of projections passes to motor nuclei that initiate digestive reflexes. There are several of these ‘cephalic phase’ reflexes whereby the brain elicits a preemptory digestive response to prepare for the food that it is simultaneously ordering to be swallowed. These reflexes are mediated by the vagus (Lat: wandering) nerve that ramifies throughout the viscera.

2.3 Discrimination Of Quality And Intensity

A third projection from brain stem taste areas passes up to the thalamus and cortex of the forebrain. Neurophysiological recordings from macaques indicate that taste quality and intensity are represented most accurately in primary taste cortex (Scott and Plata-Salaman 1999). Therefore, the capacity to identify a substance in the mouth most likely derives from cortical activity.

2.4 Hedonic Appreciation

The degree to which a taste is appealing or repulsive— its hedonic tone—is determined by projections from primary taste cortex to other cortical and subcortical sites. Prominent among these are secondary taste cortex in the orbitofrontal region, the amygdala, and the hypothalamus. In macaques, neurons in these areas respond briskly to the taste of glucose when the animal is hungry. As he feeds and becomes satiated, the neurons show progressively less response. The appeal of glucose declines in parallel, finally to turn to rejection as these hedonic neurons fail to respond (Rolls 1995). Even then, however, other tastes may activate these cells and restore the macaque’s eagerness to eat. Similarly, humans may be surfeited by a main course, yet show renewed enthusiasm as dessert arrives. It is this enduring sense of pleasure that extends the reflexive bite to a meal; a meal to a diet.

3. Basic Taste Qualities

It remains controversial whether there are basic taste qualities, though most scientists accept the notion at least as a convenient means of organizing the system. The number and identity of the basic tastes is also at issue. Criteria for acceptance include (a) having a specialized transduction mechanism for recognition at the receptor level, (b) eliciting a pattern of neural activity that is distinct from, and does not cross-adapt with, those of other basic taste stimuli, and (c) evoking a taste perception that is unique (in humans) and which does not generalize to those of other tastes (in lower animals). Sweet (glucose, sucrose), salty (NaCl), sour (HCl, citric acid), and bitter (quinine) arouse little debate, and are held by some to comprise the complete range of taste perceptions. Others argue for the inclusion of the amino acid taste umami (Japanese, roughly translated as savory, represented by monosodium glutamate), which they deem to satisfy the criteria above. Less well-developed cases are presented for the taste of fats and for complex carbohydrates or starches.

4. Taste Receptors

4.1 Anatomy

Humans have about 300,000 taste receptor cells, though the number may vary by a factor of 100 across individuals. They are gathered in groups of about 50 into goblet-shaped structures called taste buds, which number some 6,000. Two-thirds of the buds are located on the surface of the tongue, housed in groups of 3 to 250 in small mounds called papillae (Lat: nipple). Each of the three types of papillae covers a discrete area of the tongue. At the front are 200 fungiform (Lat: mushroom-shaped) papillae, each containing from 0–36 taste buds with an average of three. On each side are about six foliate (Lat: leaf-shaped) papillae, each housing some 100 buds. Toward the back are typically nine circumvallate (Lat: surrounded by a trench) papillae each containing 250 buds. This brings the total number of buds on the tongue to about 4,000. Another 2,000 are not gathered into papillae, but are embedded in the epithelium of the soft palate, pharynx, larynx, and epiglottis (Fisher and Scott 1997).

4.2 Transduction Mechanisms

4.2.1 Sweet Taste. Sweetness signals the availability of immediate energy. While sugars are not as dense a caloric source as are fats, they are useful to the brain and muscles only minutes after consumption, and so play a crucial role in survival. Consequently, sweetness has a powerful hedonic appeal, and the word itself has become synonymous with pleasure.

Sugars and most other sweet molecules bind with specific—though as yet unidentified—proteins on taste receptor cells. Once activated, these receptors stimulate G-proteins to amplify the signal. This activates the enzyme adenylate cyclase (AC) which converts ATP to cAMP. It is cAMP that serves as the second messenger, causing protein kinase A (PKA) to close the potassium (K) channels of the cell’s membrane. The positively-charge K ions that would otherwise exit through the membrane are instead sequestered within it, depolarizing the cell and causing calcium ion channels to open. This is the event that releases neurotransmitter from the taste receptor onto the peripheral nerve terminals, initiating the signal that is carried to the central nervous system.

4.2.2 Salt Taste. Sodium (Na, Lat: natrium) is the crucial ion for controlling movement of body fluids by means of the osmotic force it exerts, and for carrying electrical currents through its positive charge. Its loss devastates normal physiological function. As sodium concentration declines from 140 to below 115 mM, cardiovascular and muscular processes are compromised, and with them the animal’s speed and endurance. With further loss, sodium is unavailable to carry electrical potentials resulting in neurological symptoms of stupor, convulsions, and coma. The management of sodium stores is, thus, central to an animal’s existence. Accordingly, there is a powerful selection pressure to detect sodium, and reward associated with its taste up to isotonic concentrations.

Sodium enters and activates taste cells simply by passing through ion channels along its concentration gradient. The positive charge the ion carries serves to depolarize the cell and so generates action potentials and transmitter release. These ions are then extruded by Na K transporters to re-establish the resting state of the receptor.

This occurs readily at the top of the cell where its membrane is exposed to saliva. Access to sodium channels along its side is more controversial. There are tight junctions between taste cells that have been thought to prevent molecules from passing down their sides. This turns out not to be the case for the small, mobile sodium ion. However, the degree to which sodium can gain access to side channels depends on the anion with which it is paired. Chloride is nearly as small as sodium, passes through the tight junction with it, and allows sodium extensive contact with side channels. Larger anions such as acetate or gluconate are blocked by the tight junction. The negative charge that builds up at this barrier holds the positively charged sodium ion close and prevents it from reaching side channels. Accordingly, the larger the anion, the weaker the salt taste.

4.2.3 Sour (Acid) Taste. Sourness is the recognition of protons (H+). These ubiquitous ions participate in many physiological processes. They are also plentiful in unripe fruit and spoiled food, and so serve to warn the animal of danger. These two roles make the recognition of protons a central feature of all chemosensory systems, from protozoans to humans.

The small, mobile proton can penetrate ion channels on all parts of the receptor, and once inside they can affect cellular processes in several ways. Thus, the mechanisms of acid transduction should be varied and subtle. One path has been established and another hypothesized. In amphibians, protons block leaky potassium channels, restricting potassium to the cell and so causing depolarization. In mammals, it is hypothesized that protons enter and so depolarize the cell via sodium channels. This raises an issue of sensory coding that has not yet been addressed, namely, how the animal can discriminate between sour and salty tastes if protons and sodium—both monovalent cations—activate the same receptors by means of the same mechanism. The implication is that other transduction processes for acids remain to be discovered.

4.2.4 Bitter Taste. Plants defend themselves against foragers with toxins. Some 10 percent of plant species contain alkaloids, and toxic glycosides are still more common. Animals counter by developing detectors of toxins which, when activated, usually generate a bitter taste and rejection response.

Toxins comprise a variety of molecular structures and disrupt animal physiology in many ways. The taste system cannot focus on a particular molecule, but rather must attend to the common physiological outcome of toxicity. Thus, there will be multiple transduction mechanisms for bitter stimuli. Since most toxic molecules are organic, specialized protein receptors and second messenger systems are likely.

Three mechanisms for bitter molecules have been identified. First, like protons, bitter salts and quinine block leaky potassium channels, restricting potassium to the cell and causing depolarization. How the animal can discriminate bitter from sour when protons use the same mechanism is not known. Second, alkaloids are thought to bind with an undiscovered protein receptor whose activation is amplified by a G-protein. This stimulates the enzyme phosphodiesterase to block cAMP production, a process that could disinhibit calcium channels that are normally held in check by cAMP. The entry of calcium would depolarize the cell and cause transmitter release. Third, bitter stimuli are transduced through the inositol triphosphate (IP3) second messenger system. The protein receptor, coupled through a G-protein, activates phopholipase C (PLC), the enzyme that produces IP3. This second messenger then causes the release of calcium from stores sequestered within the cell, resulting in depolarization and release of transmitter. Most toxins are transduced by more than one of these mechanisms. Animals build redundancy into their capacity to detect poison (Lindemann 1996).

5. Neural Coding

Once transduced, taste information must be encoded in a neural signal that travels to the central nervous system for processing and interpretation. The nature of that code and the organization of the neurons that generate it have been sources of debate for decades.

5.1 Gustatory Neuron Types

Most researchers accept that taste neurons may be divided into three or four discrete types according to the profiles of activity they give in response to a battery of stimuli. Sweet cells and salt cells are clearly identifiable. Acid cells and quinine cells overlap more, and whether they are discrete from one another is doubtful. The centrist position is that taste neurons are of three types: sweet, salt, and generalist, with the last showing almost equal sensitivity to all qualities except sweetness (Smith and Shepherd 1999).

5.2 The Code For Taste Quality

The nature of the neural code for taste has been the central controversy of the field for decades. The two positions have come to be called labeled-line and across-fiber patterning.

5.2.1 Labeled-Line Theory. Proponents of labeledline theory contend that there is a small number of discrete basic tastes, each served by an associated neuron type. All neurons of one type are dedicated to and responsible for the recognition of their assigned basic taste. Hence, their communication channels—their lines—may be labeled with that quality. In this view, there are four independent systems whose transduction mechanisms, structures, connections, functions, and very reasons for being may be studied in isolation.

5.2.2 Across-fiber Patterning. Neuroscientists had anticipated a labeled-line code for taste from the work of nineteenth century psychophysicists, who concluded that taste was reducible to a small number of independent qualities. The first electrophysiological recording from taste nerve fibers violated that anticipation (Pfaffmann 1941). Single fibers of taste nerves were broadly responsive across the basic taste stimuli, rendering it unlikely that any one fiber would bear responsibility for signaling one taste. A code that involved a pattern of activity across fibers emerged as a more reasonable alternative. In its pure form, patterning theory holds that all neurons contribute equally to the code for each taste. A neuron makes its contribution to the code by filling one place in the activity pattern whose shape represents the taste.

While the theoretical distinctions between labeledline and patterning are clear, the empirical differences are not. Both accommodate most data. Similar taste stimuli elicit highly correlated patterns of activity, but they do so from a common set of neurons. A patterning theorist does not recognize the need for a channel in this scheme, while a labeled-line proponent sees need for only the appropriate channel and nothing else. Still, the same set of neurons, channel or not, is generating most of the activity.

The original finding of breadth of sensitivity in individual taste cells is the irrefutable evidence that favors patterning. Because a neuron responds to multiple taste qualities, its activity is only interpretable in the context provided by the responses of other neurons. A salt neuron may give the same response to a weak salt and to a strong acid. Only by comparing the response to that being given simultaneously by acid cells can it be interpreted. There may be taste neuron types and even coding channels, but they cannot operate in isolation. Taste in the central nervous system must be an integrated sense rather than a federation of four independent systems.

6. The Reward Of Taste

Eating is fundamentally a process of turning ‘other’ into ‘self.’ The raw materials for doing so—carbohydrates, proteins, fats, sodium—must come from the diet. The taste system is charged with identifying them and with providing the reward that motivates their consumption. Cloaked though it may be in table manners, the primitive, taste-inspired reward of eating nutritious foods is irresistible to many.

In modern developed societies, however, taste is viewed paradoxically as an enemy to good health. This is not because the taste system has changed, but rather the definition of health. Where once it was sufficient strength through the childbearing years, it is now clear arteries at age 70. Technical advances in recent centuries have provided nutrients in unprecedented quantity. The over consumption that followed revealed a set of pathologies that had played little role in evolutionary selection: cardiovascular disease, adultonset diabetes, hypertension, and joint problems. Taste, tuned so exquisitely to the chemical environment in which it evolved, now clashes with the very society that has learned to pander to, and profit from it. The biological reward of eating is dulled by the social disgrace of gluttony, and by the deleterious effects on health that appear only at ages our ancestors never achieved.

Bibliography:

  1. Fisher C, Scott T R 1997 Food Flavours: Biology and Chemistry. Royal Society of Chemistry, Cambridge, UK
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  4. Pfaffmann C 1941 Gustatory afferent impulses. Journal of Cellular Composition Physiology 17: 243–58
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