Ion channels and taste.
1992
Avenet P.
Ion channels are involved in all aspects of the physiology of taste cells, as demonstrated by patch clamp data obtained by several research groups over the past five years. Voltage-gated Na and K currents are responsible for the action potentials of taste cells, and Ca currents are probably responsible for transmitter release. Action potentials have been shown to be the regular response to salt, sour, and sweet in noninvasive recording experiments performed on intact mammalian tongues. Ion channels are also involved in the transduction mechanism of these taste modalities. In frog taste cells, a nonselective, amiloride-blockable channel with a conductance of 1 to 2 pS is responsible for the salt taste. An amiloride-sensitive Na current has also been demonstrated in isolated rat taste cells, though this channel is different from the one found in the frog. In mudpuppies, sour taste is mediated by a proton block of voltage-dependent K channels localized in the taste cell apical membrane. At least one of the sweet taste mechanisms utilizes cyclic adenosine monophosphate as an intracellular messenger. Intracellular cyclic adenosine monophosphate, shown to increase in taste cells in response to sweet stimuli, causes a K channel, with a conductance of 44 pS, to be closed by phosphorylation. Amino acids in the catfish are detected by a receptor-gated channel that has been reconstituted in bilayer membranes. The bitter taste of denatonium chloride does not involve a membrane conductance change but is mediated through an IP3-induced increase of intracellular Ca. Thus a diversity of mechanisms and ion channels is responsible for the detection of a diversity of taste modalities.
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