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首页> 外文期刊>BMC Neuroscience >Voltage-gated sodium channels in taste bud cells
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Voltage-gated sodium channels in taste bud cells

机译：味蕾细胞中的电压门控钠通道

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Background Taste bud cells transmit information regarding the contents of food from taste receptors embedded in apical microvilli to gustatory nerve fibers innervating basolateral membranes. In particular, taste cells depolarize, activate voltage-gated sodium channels, and fire action potentials in response to tastants. Initial cell depolarization is attributable to sodium influx through TRPM5 in sweet, bitter, and umami cells and an undetermined cation influx through an ion channel in sour cells expressing PKD2L1, a candidate sour taste receptor. The molecular identity of the voltage-gated sodium channels that sense depolarizing signals and subsequently initiate action potentials coding taste information to gustatory nerve fibers is unknown. Results We describe the molecular and histological expression profiles of cation channels involved in electrical signal transmission from apical to basolateral membrane domains. TRPM5 was positioned immediately beneath tight junctions to receive calcium signals originating from sweet, bitter, and umami receptor activation, while PKD2L1 was positioned at the taste pore. Using mouse taste bud and lingual epithelial cells collected by laser capture microdissection, SCN2A, SCN3A, and SCN9A voltage-gated sodium channel transcripts were expressed in taste tissue. SCN2A, SCN3A, and SCN9A were expressed beneath tight junctions in subsets of taste cells. SCN3A and SCN9A were expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells. HCN4, a gene previously implicated in sour taste, was expressed in PKD2L1 cells and localized to cell processes beneath the taste pore. Conclusion SCN2A, SCN3A and SCN9A voltage-gated sodium channels are positioned to sense initial depolarizing signals stemming from taste receptor activation and initiate taste cell action potentials. SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells.
机译：背景技术味蕾细胞将有关食物含量的信息从根尖微绒毛中嵌入的味觉受体传递到支配基底外侧膜的味觉神经纤维。尤其是，味觉细胞会消极化，激活电压门控的钠通道，并响应促味剂起火作用。最初的细胞去极化可归因于甜味，苦味和鲜味细胞中通过TRPM5引起的钠流入，以及表达候选酸味受体PKD2L1的酸性细胞中通过离子通道的未确定阳离子流入。尚不知道电压门控性钠通道的分子身份，该通道感应去极化信号并随后启动将味觉信息编码到味觉神经纤维的动作电位。结果我们描述了从根尖到基底外侧膜域的电信号传输所涉及的阳离子通道的分子和组织学表达谱。 TRPM5直接位于紧密连接的下方，以接收源自甜味，苦味和鲜味受体激活的钙信号，而PKD2L1则位于味觉孔处。使用通过激光捕获显微切割术收集的小鼠味蕾和舌上皮细胞，SCN2A，SCN3A和SCN9A电压门控钠通道转录物在味觉组织中表达。 SCN2A，SCN3A和SCN9A在味觉细胞子集中的紧密连接下表达。 SCN3A和SCN9A在TRPM5细胞中表达，而SCN2A在TRPM5和PKD2L1细胞中表达。 HCN4是一种先前与酸味有关的基因，在PKD2L1细胞中表达，并位于味觉孔以下的细胞过程中。结论SCN2A，SCN3A和SCN9A电压门控钠通道的位置可感测源自味觉受体激活的初始去极化信号并启动味觉细胞动作电位。 SCN2A，SCN3A和SCN9A基因产物可能解释了味觉受体细胞中河豚毒素敏感性钠电流。

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