Signal transduction and information processing in mammalian taste buds

Abstract

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 acidsensitive 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.

Caffeine induces gastric acid secretion via bitter taste signaling in gastric parietal cells

“…Activation of these receptors results, either by Gs-and adenylyl cyclase/cAMP-or by Gq-and phospholipase C (PLC)/IP 3 /Ca 2+ -dependent pathways, in the activation of the H + ,K + -ATPase, which pumps protons into the stomach lumen (22). In taste cells located on the tongue, the signaling cascade of TAS2Rs also includes a cAMP-dependent and a PLCβ2/IP3/Ca 2+ -dependent pathway (23). Initiation of the latter major pathway leads to calcium release from intracellular compartments, which in turn activates transient receptor potential M5 ion channels.…”

“…Initiation of the latter major pathway leads to calcium release from intracellular compartments, which in turn activates transient receptor potential M5 ion channels. These channels mediate an influx of sodium ions and membrane depolarization (23), leading to ATP release and bitter perception. The α-subunit of gustducin has been described to stimulate Significance This study shows that caffeine's effect on gastric acid secretion (GAS) is more complex than has been previously thought.…”

The K + channel K IR 2.1 functions in tandem with proton influx to mediate sour taste transduction

“…It was noted nearly a century ago that at the same pH, organic weak acids evoke a more intense sour sensation than strong mineral acids (18). This has been attributed to the ability of weak acids, in the protonated form, to penetrate the cell membrane, and upon entering the cell, release a proton (28). Cytosolic acidification could then affect membrane excitability and/or transmitter release.…”

“…1 A and B). To acidify the cell cytosol, we used acetic acid (AA) and propionic acid (PA), weak acids that partition in the lipid bilayer in their protonated form and are able to shuttle protons across the cell membrane (26)(27)(28). Each acid was used at a concentration of 100 mM and pH of 7.4, which generates ∼0.3 mM of the membrane permeable form.…”

“…Intracellular acidification could generate membrane depolarization either by activating excitatory, Na + -or Ca 2+ -permeable, channels, or by inhibiting K + channels (3,28). We previously tested whether weak acids could activate an inward Na + -or Ca 2+ -permeable current in PKD2L1 cells and failed to find any difference in the magnitude or reversal potential of the inward current evoked in response to pH 5 with or without acetic acid (16).…”