The mechanisms responsible for taste signal transductions are very complex. A key molecule, α-gustducin, a primarily taste-specific G protein α-subunit, was discovered in 1992 and was later found to be involved in both bitter and sweet taste transduction. A proposed mechanism for α-gustducin involves coupling specific cell-surface receptors with a cyclic nucleotide phosphodiesterase which would open a cyclic nucleotide-suppressible cation channel leading to influx of calcium, and ultimately leading to release of neurotransmitter. Although "knock-out" animals deficient in the α-gustducin gene clearly demonstrate that gustducin is an essential molecule for tasting certain bitter and sweet compounds, the precise role of α-gustducin in bitter and sweet taste is presently unclear. Indeed, there are several other signaling mechanisms in sweet and bitter taste, apparently unrelated to α-gustducin, that increase cyclic AMP or inositol 1,4,5 trisphosphate. Thus, proposed models for α-gustducin and those found by other laboratories may be parallel and interdependent.
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