Receptor cells, taste

As early as 1848, it had been suggested that sensory receptors transduce only one sensation, independent of the manner of stimulation. Behavioral experiments tend to support this theory. In 1919, Renqvist proposed that the initial reaction of taste stimulation takes place on the surface of the taste-cell membrane. The taste surfaces were regarded as colloidal dispersions in which the protoplasmic, sensory particles and their components were suspended in the liquor or solution to be tested. The taste sensation would then be due to adsorption of the substances in the solution, and equal degrees of sensation would correspond to adsorption of equal amounts. Therefore, the rate of adsorption of taste stimulants would be proportional to the total substances adsorbed. The phenomenon of taste differences between isomers was partly explained by the assumption that the mechanism of taste involves a three-dimensional arrangement for example, a layer of fatty acid floating on water would have its carboxylic groups anchored in the water whereas the long, hydrocarbon ends would project upwards. 

The speed with which taste stimulation occurs, coupled with the fact that stimulation with toxic substances does no damage to the receptors, led Beidler to suggest that taste stimulus need not enter the interior of the taste cell in order to initiate excitation. Because a taste cell has been shown to be sensitive to a number of taste qualities, and to a large number of chemical stimuli, he and his coworkers concluded that a number of different sites of adsorption must exist on the surface of the cell. Therefore, they assumed that taste response results from adsorption of chemical stimuli to the surface of the receptor at given receptor sites. This adsorption is described by a monomolecular reaction similar to that assumed by Renqvist, Lasareff, and Hahn, but with a difference. From the fact that each type of chemical-stimulus compound has a unique level of saturation of the taste receptor, it was concluded that the magnitude of the response is dependent on the initial reaction with the receptor, and not on other, subsequent receptor-reactions that are common to all types of receptor stimulation. Therefore, it was assumed that the magnitude of neural response is directly proportional to the number of sites filled, the maximum response occurring when all of the sites are filled. Beidler derived a fundamental... 

The events that follow the initial adsorption of the taste stimulus to the receptor matrix of the taste-cell membrane are conformational changes in... 

Fig. 1.—Diagrammatic Representation of the Three Steps in the Taste-cell Transduction. Step 1, interaction of stimulus (S) with membrane-bound receptor (R) to form stimulus-receptor complex (SR) step 2, conformational change (SR) to (SR), brought about by interaction of S with R (this change initiates a change in plasma-membrane conformation of taste cells, probably below the level of the tight junction) and step 3, conformational changes of the membrane result in lowered membrane resistance, and the consequential influx on intracellular ionic species, probably Na. This influx generates the receptor potential which induces synaptic vesicular release to the innervating, sensory nerve, leading to the generator potential.

That the initial event of taste stimulation takes place on the cell surface of the taste receptor is now universally accepted. In addition, accumulated evidence strongly suggests that taste-bud stimulation is extracellular in nature. For example, (1) the sweet-taste response is both rapid and reversible, (2) the intensely sweet proteins monellin" and thaumatin could not possibly penetrate the cell, because of their size, and (3) miraculin, the taste-modifying glycoprotein, having a molecular weight of 44,000 would also be too large to penetrate the taste cell. ... 

Taste receptor cells are organized into taste buds 825 Sensory afferents within three cranial nerves innervate the taste buds 826 Information coding of taste is not strictly according to a labeled line 826 Taste cells have multiple types of ion channels 826 Salts and acids are transduced by direct interaction with ion channels 826 Taste cells contain receptors, G proteins and second-messenger-effector enzymes 827... 

FIGURE 50-7 Rattongue, taste papillae and taste buds. (A) Surface of the rat tongue showing location of the taste papillae. (B) Cross-section of the three main types of taste papillae fungiform, foliate and vallate. (C) The taste bud contains 50-100 taste cells, including receptor cells and basal cells. 

The detailed mechanism of its taste-inducing behavior is still unknown. It has been suggested that the miraculin molecule can change the structure of taste cells on the tongue. As a result, the sweet receptors are activated by acids, which are sour in general. This effect remains until the taste buds return to normal. 

The taste cells are situated in the lingual epithelium with the apical membrane exposed to the mucosal surface of the oral cavity and the basal surface in contact with the nerve [interstitial fluid] [FIGURE 10]. Within the basolateral surface are the nerves which respond to the chemestiietic stimulants, i.e. direct nerve stimulation. The microvilli at the apical membrane contain receptor proteins which respond to sweeteners, some bitters and possibly coolants. The olfactory cells are bipolar neurons with dendritic ends containing cilia exposed to the surface and axons linked to the brain, where they synapse in the olfactory bulb. The transfer of information from this initial stimulus-receptor interaction to the brain processing centers involves chentical transduction steps in the membrane and within the receptor cells. The potential chemical interactions at the cell membrane and within the cell are schematically outlined in FIGURE 10. 

FIGURE 10. A) Schematic of taste cell embedded in epithelium. Shown are the apical membrane which contains the microvilli and the basal membrane which synapses with the nerve B) Stimulus can interact with a receptor protein embedded in membrane which activates G-protein, with the membrane or directly with an ion channel protein C) GTP stimulation of phosphatase for formation of cAMP or IP3 and opening of ion channel (Adapted from ref. 2). 

Recently, studies were reported measuring the kinetics of stimulation of both cAMP and 3 using a mixing device and rapid quenching, in the millisecond range, in rat olfactory cilia (67). The response to a mixture of < orants peaks within 25 to 50 milliseconds, the time frame expected for receptors, with both cAMP and IP3. Similar measurements of the change in concentration of cAMP or IP3 were also done in the taste cell. Here mice, which were bred as bitter tasters and nontasters , were used as subjects. The bitter stimuli, sucrose octaacetate, strychnine and denatonium benzoate, were shown to increase IP3 levels in a membrane preparation from "taster" mice in the presence of GTP-protein and Ca but not in membranes from "nontaster" mice (68). 

Intracellular recordings from taste cells of rat and hamster show that even primary receptor cells are sensitive tu three or four of the so-called basic taste modalities. Consequently, it is generally held that a variety or dilferem receptor sites commonly exist on the receptor membrane of anyone receptor cell. Biochemical characterization or events at receptor sites has progressed in analyzing electrolyte and carbuhydrate stimulation. 

One method to realize the taste sensor may be the utilization of similar materials to biological systems as the transducer. The biological membrane is composed of proteins and lipids. Proteins are main receptors of taste substances. Especially for sour, salty, or bitter substances, the lipid-membrane part is also suggested to be the receptor site [6]. In biological taste reception, taste stimulus changes the receptor potentials of taste cells, which have various characteristics in reception [7,8]. Then the pattern constructed of receptor potentials is translated into the excitation pattern in taste neurons (across-fiber-pattem theory). 

The taste receptor mechanism has been more fully described by Kurihara (1987). The process from chemical stimulation to transmitter release is schematically presented in Figure 7-4. The receptor membranes contain voltage-dependent calcium channels. Taste compounds contact the taste cells and depolarize the receptor membrane this depolarization spreads to the synaptic area, activating the voltage-dependent calcium channels. Influx of calcium triggers the release of the transmitter norepinephrine. 

Taste transduaion is initiated when taste stimuli interact with exposed cells in the apical microvilli of the tongue. The receptor-ligand interaction leads to membrane depolarization and to activation of afferent gustatory neurons. The perception of the common human taste qualities— sweet, bitter, salty, and sour—has been assigned to groups of taste neurons. But a characteristic property of taste transduction is that the taste cells can also be stimulated directly without the intervention of receptors. 

Zhao GQ, Zhang Y, Hoon MA, Chandrashekar J, Erlenbach I, 29. Ryba NJ, Zuker CS. The receptors for mammalian sweet and umami taste. Cell 2003 115 255-266. 

Maruyama Y, Pereira E, Margolskee RF, Chaudhari N, Roper SD. Umami responses in mouse taste cells indicate more than one receptor. J. Neurosci. 2006 26 2227-2234. 

Hofer D, Puschel B, Drenckhahn, D. Taste receptor-hke cells in the rat gut identified by expression of alpha-gustducin. Proc. Natl. Acad. Sci. U. S. A. 1996 93 6631-6634. 

---