Spielman A I
New York University College of Dentistry, Basic Science Division, New York 10010, USA.
J Dent Res. 1998 Apr;77(4):539-44. doi: 10.1177/00220345980770040601.
The mechanisms responsible for taste signal transductions are very complex. A key molecule, alpha-gustducin, a primarily taste-specific G protein alpha-subunit, was discovered in 1992 and was later found to be involved in both bitter and sweet taste transduction. A proposed mechanism for alpha-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 alpha-gustducin gene clearly demonstrate that gustducin is an essential molecule for tasting certain bitter and sweet compounds, the precise role of alpha-gustducin in bitter and sweet taste is presently unclear. Indeed, there are several other signaling mechanisms in sweet and bitter taste, apparently unrelated to alpha-gustducin, that increase cyclic AMP or inositol 1,4,5 trisphosphate. Thus, proposed models for alpha-gustducin and those found by other laboratories may be parallel and interdependent.
负责味觉信号转导的机制非常复杂。1992年发现了一种关键分子——α-味导素，它是一种主要的味觉特异性G蛋白α亚基，后来发现它参与苦味和甜味转导。α-味导素的一种推测机制涉及将特定的细胞表面受体与一种环核苷酸磷酸二酯酶偶联，该酶会打开一个可被环核苷酸抑制的阳离子通道，导致钙离子内流，并最终导致神经递质释放。尽管缺乏α-味导素基因的“基因敲除”动物清楚地表明味导素是品尝某些苦味和甜味化合物的必需分子，但α-味导素在苦味和甜味中的精确作用目前尚不清楚。事实上，在甜味和苦味中还有其他几种信号转导机制，显然与α-味导素无关，它们会增加环磷酸腺苷或肌醇三磷酸。因此，α-味导素的推测模型与其他实验室发现的模型可能是平行且相互依存的。
