Molecular mechanisms of ion channels and second messengers in gustatory transduction of taste cells.

1.在分析NaCI刺激引起的菌状乳头味觉细胞的内向电流时，发现小鼠的味觉细胞根据顶端受体膜上有无或几乎没有阿米洛利可阻断上皮钠通道(ENaC)而分为两种类型。当由NaCI刺激引起的大的内向电流被阿米洛利阻断时，ENaC的亚基可能由α、β和伽马组成。然而，当内向电流没有被阿米洛利完全或几乎完全阻断时，味觉细胞的顶膜很可能缺乏ENaC.2的整个亚基或β和伽马。阿米洛利完全不能阻断酸刺激引起的小鼠内向电流。因此，小鼠味觉细胞的酸反应不是通过阿米洛利可阻断的ENaC引起的。我们最近的发现表明，有两条途径可以产生酸反应。其一是质子与顶膜上的离子旋转受体的级联结合，以及阳离子通过阳离子通道的流入。另一种途径是G蛋白和效应器分子的激活、第二信使的产生以及通过蛋白激酶关闭基底外侧膜上的C_1^-通道。有两条途径与沙土鼠味觉细胞对两种甜味剂的甜味反应有关。糖刺激的一个途径是G蛋白和腺苷环化酶的级联激活，cAMP的产生，以及通过蛋白激酶关闭K+通道。非糖甜味剂的另一种途径是激活G蛋白和PLC，产生1P3，并从细胞内的Ca^2^库释放Ca^2^。

1. When inward currents in the fungiform papilla taste cells induced by NaCi stimuli were analysed, it was found that the taste cells in the mouse were divided into two types according to the presence and absence or almost absence of amiloride-blockable epithelial Na^+ channels (ENaC) in the apical receptive membrane. When large inward currents elicited by NaCi stimuli were blocked by amiloride, the subunits of ENaC may be composed of alpha, beta and gamma. However,when the inward currents were not blocked completely or almost completely by amiloride, it is likely that the apical membrane of a taste cell lacks the whole subunits or beta and gamma of ENaC.2. The inward current in the mouse induced by an acid stimulus was not blocked at all by amiloride. Therefore, the acid response of mouse taste cells is not evoked via the amiloride-blockable ENaC.Our recent finding suggests that there are two pathways for generation of acid responses. One is a cascade of binding of proton to ionotoropic receptor in the apical membrane and inflow of cations through the cation channels. The other pathway is a cascade of activation of G-protein and effector molecule, production of a second messenger and closure of C1^- channels in the basolateral membrane via a protein kinase.3. Two pathways are concerned with generation of sweet responses in gerbil taste cells for two types of sweeteners. One pathway for sugar stimuli is a cascade of activation of G-protein and adenylate cyclase, production of cAMP and closure of K^+ channels via a protein kinase. The other pathway for non-sugar sweeteners is a cascade of activation of G-protein and PLC, production of 1P3 and release of Ca^2^+ from the intracellular Ca^2^+ store.