Signal transduction and information processing in mammalian taste buds.
The molecular machinery for chemosensory transduction in taste buds has received considerable attention within the last decade. Consequently, we now know a great deal about sweet, bitter, and umami taste mechanisms and are gaining ground rapidly on salty and sour transduction. Sweet, bitter, and umami tastes are transduced by G-protein-coupled receptors. Salty taste may be transduced by epithelial Na channels similar to those found in renal tissues. Sour transduction appears to be initiated by intracellular acidification acting on acid-sensitive membrane proteins. Once a taste signal is generated in a taste cell, the subsequent steps involve secretion of neurotransmitters, including ATP and serotonin. It is now recognized that the cells responding to sweet, bitter, and umami taste stimuli do not possess synapses and instead secrete the neurotransmitter ATP via a novel mechanism not involving conventional vesicular exocytosis. ATP is believed to excite primary sensory afferent fibers that convey gustatory signals to the brain. In contrast, taste cells that do have synapses release serotonin in response to gustatory stimulation. The postsynaptic targets of serotonin have not yet been identified. Finally, ATP secreted from receptor cells also acts on neighboring taste cells to stimulate their release of serotonin. This suggests that there is important information processing and signal coding taking place in the mammalian taste bud after gustatory stimulation.
Roper
Stephen D
SD
Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA. roper@miami.edu
D000143:Acids / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D002450:Cell Communication / Q000187:drug effects / Q000502:physiology; D062708:Epithelial Sodium Channel Agonists; D053503:Epithelial Sodium Channels / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000819:agonists / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000819:agonists / Q000502:physiology; D015290:Second Messenger Systems / Q000502:physiology*; D012701:Serotonin / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D012970:Sodium Glutamate / Q000494:pharmacology; D013268:Stimulation, Chemical; D013395:Sucrose / Q000494:pharmacology; D009435:Synaptic Transmission / Q000502:physiology*; D013649:Taste / Q000502:physiology*; D013650:Taste Buds / Q000166:cytology / Q000502:physiology*
D000143:Acids; D062708:Epithelial Sodium Channel Agonists; D053503:Epithelial Sodium Channels; D007473:Ion Channels; D018377:Neurotransmitter Agents; D043562:Receptors, G-Protein-Coupled; D017673:Sodium Chloride, Dietary; D012701:Serotonin; D013395:Sucrose; D000255:Adenosine Triphosphate; D012970:Sodium Glutamate