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烟碱样乙酰胆碱受体（Acetylcholine receptor,AChR）是由4种亚基组成的五聚体,其表达受神经电活动控制。胚胎期神经植入前,AChR弥散分布于肌细胞表面;突触发生后,突触外AChR表达受抑制,而集中于突触后膜表达。出生后去神经或用特异的Na~+通道阻断剂阻断电活动可引起骨骼肌组织突触外AChR mRNA明显升高。电刺激去神经的肌肉又可使突触外AChR基因表达关闭。因此,有关膜去极化与AChR基因转录激活的偶联机制研究已成为当前愈发感兴趣的课题。Klarsfeld等利用特异的阻断剂证明,电活动抑制AChR的生物合成涉及Ca~（2+）和PKC的作用。huang等发现,Ca~（2+）通过去极化的膜由L型钙离子通道进入胞浆,可引起AChR基因快速失活;膜去极化可引起核内PKC活性升高,进而导致AChR基因表达所必需的1个因子磷酸化而失活。Neville等根据神经和电刺激后基因表达动力
Acetylcholine receptor (AChR) is a pentamer composed of four kinds of subunits whose expression is controlled by neural electrical activity. AChR diffusely distributed on the surface of muscle cells before implantation of embryonic nerves. After synapse was produced, the expression of AChR was inhibited in synapse but concentrated in the postsynaptic membrane. Denervation after birth or with specific Na ~ + channel blocker blocking electrical activity can cause skeletal muscle AChR mRNA significantly increased. Electrical stimulation of the denervated muscle can turn off the expression of extra-AChR genes. Therefore, studies on the coupling mechanism of membrane depolarization and AChR gene transcription and transcription have become more and more interesting subjects. Klarsfeld et al. Used specific blockers to demonstrate that electrical activity inhibits the biosynthesis of AChRs involved in Ca 2+ and PKC. huang et al. found that Ca 2+ could enter the cytoplasm through the L-type Ca 2+ channel through depolarizing membrane and cause rapid inactivation of AChR gene. Membrane depolarization could cause the increase of PKC activity in the nucleus, leading to AChR One of the factors necessary for gene expression is phosphorylated and inactivated. Neville and others based on nerve and electrical stimulation of gene expression after power