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.

中文翻译：

---

品味接待。

关于周围味觉的细胞机制的最新研究已经定义了涉及膜受体，G蛋白，第二信使和离子通道的转导途径。有机促味剂的受体受到了广泛关注，因为它们提供了反应的特异性。他们未来的克隆将构成重大进步。味觉转导通常并行利用两个或多个途径。例如，大鼠的对甜味敏感的味觉细胞似乎会通过激活腺苷酸环化酶来响应蔗糖，随后是腺苷3'，5'-环一磷酸（cAMP）依赖性膜事件和Ca2 +吸收。相同的细胞对某些人造甜味剂的反应不同，即激活磷脂酶C（PLC），然后从细胞内储存释放肌醇1,4,5-三磷酸（IP3）依赖性Ca2 +。一些苦味剂会阻断K +通道或引发级联受体G1蛋白，PLC，IP3和Ca2 +释放，或引发级联受体α-gustducin，磷酸二酯酶（PDE），cAMP降低和cAMP阻断通道的开放。膜渗透性苦味剂可通过与上述级联反应的G蛋白，PLC或PDE相互作用引发细胞应答。盐的味道是由电流通过位于顶膜的阳离子通道流入味觉细胞而引发的，即使基底外侧通道也可能起作用（跟随盐通过旁细胞途径扩散）。在啮齿动物中，盐味的Na +特异性成分通常是由顶端阿米洛利敏感的Na +通道介导的，但除此之外，还存在特异性较低而不对阿米洛利敏感的味道成分。酸味可能部分是由传导质子的阿米洛利敏感的Na +通道介导的，但其他机制无疑也起作用。因此，味觉细胞的转导通常包括平行的途径。此外，转导途径随味蕾在舌头上的位置而变化，当然，跨动物物种也不同。识别这些途径，了解它们如何被控制以及为什么它们演变成这种复杂性是当前研究的主要目标。