Sodium ions are largely responsible for establishing a salty taste. Sodium ions diffuse through the pore of the taste bud and enter the taste receptor cell through sodium-selective channels present in the cell membrane. These channels are characterized by their sensitivity to the drug amiloride and their insensitivity to changes in voltage. Thus, they are different from the sodium channels involved in propagation of action potentials. The entry of positively charged ions depolarizes the taste receptor cell, opens voltage-dependent calcium channels, and increases the influx of calcium, thereby allowing calcium to enter the cell and cause release of neurotransmitter.


A sour taste is associated with acidic substances that affect sour-sensitive taste receptors in two ways: (1) Acids in solution generate hydrogen ions that can permeate the amiloride-sensitive sodium channel described earlier and cause depolarization-stimulated release of neurotransmitter in the same manner as sodium ions. (2) Hydrogen ions also block a potassium-selective channel within the membrane which also causes depolarization because the normal movement of potassium out of the cell is blocked, and more positively charged potassium ions are trapped intracellularly. Foods that cause depolarization and increased transmitter release through both of these mechanisms are perceived as sour; those that cause depolarization only through diffusion of cations through the sodium channel are perceived as salty.


Specific membrane receptor proteins on some taste cells bind sugars and other sweet-tasting substances. Binding to these receptor sites activates a second-messenger system similar to the one associated with noradrenergic receptors. The receptor is coupled to a G-protein that activates protein kinase A and causes it to phosphorylate and block a potassium-selective channel. As a result, sweet-sensitive taste cells are depolarized.


Because many toxic compounds have an unpleasant bitter taste, receptor cells that respond to bitter substances can function as poison detectors; however, some bitter foods are not necessarily unpleasant or toxic (e.g., quinine and caffeine, although one might argue the latter point for caffeine). Several different transduction mechanisms are involved in detection of bitterness in food. Some bitter compounds (e.g., calcium ions and quinine) decrease conductance of potassium-selective channels similar to the mechanisms used for detection of sweetness. Other bitter substances bind to specific membrane receptors that activate second-messenger systems and cause membrane depolarization. One type of bitterness receptor triggers an increased production of the intracel-lular messenger inositol triphosphate (IP3). In all other transduction mechanisms described earlier, depolarization of the receptor cell causes an increase in calcium influx through voltage-sensitive calcium channels, and calcium ions act as the trigger for release of neurotrans-mitter. This is not so in the case of the IP3 transduction mechanism. Here, the membrane potential is not altered; rather, IP3 causes the release of calcium from internal storage sites which in turn directly stimulates neuro-transmitter release.


The umami taste is not as familiar as the preceding four basic tastes. Nonetheless, it is discernible as a distinctive and delicious taste associated with certain amino acids such as glutamate and perhaps arginine. These amino acids bind to and activate a cation-permeable channel, causing depolarization in a manner similar to glutamate activation of cation channels in the brain.

FIGURE 6 Transduction mechanisms for salt, sour, umami, sweet, and bitter. All taste receptors release neurotransmitters in response to an increase in free intracellular calcium, usually due to depolarization that opens reactive calcium channels. The cause of this depolarization varies with the specific receptor cell. (A) Salty taste is transduced by amiloride-sensitive sodium channels that are always open. When the sodium concentration increases on the surface of the microvilli, sodium ions can enter the channels and depolarize the cell. Hydrogen ions can also enter these channels, thus acid food has a salty taste. (B) Sour taste is elicited when hydrogen ions act directly on open potassium channels, closing them and depolarizing the cell. (C) Umami taste utilizes a cation channel similar to CNS glutamate receptors. Glutamate (e.g., monosodium glutamate, or MSG) binds to the receptor and allows all small cations to pass, including sodium, potassium, and calcium. The net effect of these ionic movements is to depolarize the cell. (D) Sweet tastes, such as sugars and certain proteins, produce depolarization by a chain of events that resemble many CNS neurotransduction systems. Binding of the receptor protein activates a Gs-protein that stimulates adenylyl cyclase to produce cyclic adenosine monophosphate (cAMP), which releases protein kinase A (PKA) from its regulator proteins. PKA then phosphorylates potassium channels, closing them and depolarizing the cell. (E) There are at least two types of bitter receptors; quinine stimulates the bitter 1 receptor by simply closing potassium channels. (F) Other bitter substances bind with a bitter 2 receptor and stimulate the production of inositol triphosphate (IP3). IP3 triggers the release of calcium from internal stores, stimulating neurotransmitter release without an intervening depolarization.

A. Lateral view of cerebral cortex gustatory cortex

A. Lateral view of cerebral cortex gustatory cortex

insula exposed B. Coronal section of cerebral cortex

ventral posterior medial nucleus gustatory cortex ventral posterior medial nucleus gustatory cortex

solitary nucleus gustatory division

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