Gao Na, Lu Min, Echeverri Fernando, Laita Bianca, Kalabat Dalia, Williams Mark E, Hevezi Peter, Zlotnik Albert, Moyer Bryan D
Senomyx, Inc, 4767 Nexus Centre Drive, San Diego, CA 92121, USA.
BMC Neurosci. 2009 Mar 12;10:20. doi: 10.1186/1471-2202-10-20.
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.
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.
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.
味蕾细胞将食物成分的信息从顶端微绒毛中嵌入的味觉受体传递给支配基底外侧膜的味觉神经纤维。特别是，味觉细胞会发生去极化，激活电压门控钠通道，并对味觉刺激物产生动作电位。最初的细胞去极化归因于甜味、苦味和鲜味细胞中通过TRPM5的钠内流，以及酸味细胞中通过表达候选酸味受体PKD2L1的离子通道的未知阳离子内流。感知去极化信号并随后启动将味觉信息编码给味觉神经纤维的动作电位的电压门控钠通道的分子身份尚不清楚。
我们描述了参与从顶端膜结构域到基底外侧膜结构域电信号传递的阳离子通道的分子和组织学表达谱。TRPM5位于紧密连接的正下方，以接收源自甜味、苦味和鲜味受体激活的钙信号，而PKD2L1位于味觉孔处。使用通过激光捕获显微切割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本在味觉组织中表达。SCN2A、SCN3A和SCN9A在味觉细胞亚群的紧密连接下方表达。SCN3A和SCN9A在TRPM5细胞中表达，而SCN2A在TRPM5和PKD2L1细胞中表达。HCN4，一个先前与酸味有关的基因，在PKD2L1细胞中表达，并定位于味觉孔下方的细胞突起。
SCN2A、SCN3A和SCN9A电压门控钠通道的位置能够感知源自味觉受体激活的初始去极化信号，并引发味觉细胞动作电位。SCN2A、SCN3A和SCN9A基因产物可能是味觉受体细胞中对河豚毒素敏感的钠电流的原因。
