Lindemann B
Fachrichtung Physiologie, Universität des Saarlandes, Homburg/Saar, Germany.
Physiol Rev. 1996 Jul;76(3):719-66. doi: 10.1152/physrev.1996.76.3.719.
Recent research on cellular mechanisms of peripheral taste has defined transduction pathways involving membrane receptors, G proteins, second messengers, and ion channels. Receptors for organic tastants received much attention, because they provide the specificity of a response. Their future cloning will constitute a major advance. Taste transduction typically utilizes two or more pathways in parallel. For instance, sweet-sensitive taste cells of the rat appear to respond to sucrose with activation of adenylyl cyclase, followed by adenosine 3',5'-cyclic monophosphate (cAMP)-dependent membrane events and Ca2+ uptake. The same cells respond differently to some artificial sweeteners, i.e., with activation of phospholipase C (PLC) followed by inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release from intracellular stores. Some bitter tastants block K+ channels or initiate the cascade receptor G1 protein, PLC, IP3, and Ca2+ release or the cascade receptor alpha-gustducin, phosphodiesterase (PDE), cAMP decrease, and opening of cAMP-blocked channels. Membrane-permeant bitter tastants may elicit a cellular response by interacting with G protein, PLC, or PDE of the above cascades. Salt taste is initiated by current flowing into the taste cell through cation channels located in the apical membrane, even though basolateral channels may also contribute (following salt diffusion through paracellular pathways). In rodents, the Na+-specific component of salt taste is typically mediated by apical amiloride-sensitive Na+ channels, but less specific and not amiloride-sensitive taste components exist in addition. Sour taste may in part be mediated by amiloride-sensitive Na+ channels conducting protons, but other mechanisms certainly contribute. Thus the transduction of taste cells generally comprises parallel pathways. Furthermore, the transduction pathways vary with the location of taste buds on the tongue and, of course, across species of animals. To identify these pathways, to understand how they are controlled and why they evolved to this complexity are major goals of present research.
近期关于外周味觉细胞机制的研究已经明确了涉及膜受体、G蛋白、第二信使和离子通道的转导途径。有机味觉物质的受体备受关注，因为它们决定了反应的特异性。其未来的克隆将是一项重大进展。味觉转导通常同时利用两条或更多条途径。例如，大鼠的甜味敏感味觉细胞似乎通过激活腺苷酸环化酶对蔗糖作出反应，随后发生依赖于3',5'-环磷酸腺苷（cAMP）的膜事件和钙离子摄取。同样的细胞对一些人工甜味剂有不同反应，即通过激活磷脂酶C（PLC），随后从细胞内储存中释放出依赖于1,4,5-三磷酸肌醇（IP3）的钙离子。一些苦味物质会阻断钾离子通道或启动级联反应受体G1蛋白、PLC、IP3和钙离子释放，或者启动级联反应受体α-味导素、磷酸二酯酶（PDE）、cAMP减少以及cAMP阻断通道的开放。可透过膜的苦味物质可能通过与上述级联反应中的G蛋白、PLC或PDE相互作用引发细胞反应。咸味是由电流通过位于顶端膜的阳离子通道流入味觉细胞引发的，尽管基底外侧通道也可能起作用（在盐通过细胞旁途径扩散之后）。在啮齿动物中，咸味的钠离子特异性成分通常由顶端的氨氯地平敏感钠离子通道介导，但此外还存在不太特异且对氨氯地平不敏感的味觉成分。酸味可能部分由传导质子的氨氯地平敏感钠离子通道介导，但其他机制肯定也起作用。因此，味觉细胞的转导通常包括平行途径。此外，转导途径因味蕾在舌上的位置而异，当然也因动物物种而异。确定这些途径、了解它们是如何被控制的以及为何它们进化到如此复杂的程度是当前研究的主要目标。
