A Study on Ca Influx and Acetyulcholine Release in the Presynaptic Terminals of Cholinergic Nerve of the Electric Organ

（1）在日本电鳐电器官神经末梢突触前质膜上存在N型、P/Q型和L型电压依赖性钙通道（VDCCs）。乙酰胆碱（ACh）的释放主要由-和P/Q型VDCCs介导。（2）从电鳐电叶cDNA文库中克隆了突触素的cDNA。Synaphine与syntaxin、VAMP和SNAP-25相关，提示其参与胞吐作用。（3）从上述cDNA文库中还分离了Alzheimer’s β-淀粉样前体蛋白（APP）的cDNA。分析表明，产物蛋白APP在成熟后被磷酸化。（4）电器突触膜上存在腺苷A_1和腺苷<2B>A_2受体。后者的激活通过增强P/Q型VDCCs增加ACh释放，而前者的激活通过抑制N型VDCCs减少ACh释放。（5）Lambert-Eaton综合征（LES）患者的抗体通过特异性下调P/Q型VDCCs而减少ACh的释放。（6）用电器官突触体免疫大鼠或小鼠，建立LES动物模型。

(1)There exist N-, P/Q- and L-type voltage-dependent Ca channels (VDCCs) in the presynaptic plasma membranes of nerve terminals of the electric organ isolated from the Japanese electric ray Narke japonica. The acetylcholine (ACh) release was predominantly mediated by-and P/Q-type VDCCs. (2)cDNA for synaphine was cloned from the cDNA library prepared from the electric lobe of the ray. Synaphine was found to be associated with syntaxin, VAMP and SNAP-25, suggesting its involvement in the exocytosis. (3)cDNA for the Alzheimer's beta-amyolid presursor protein (APP) was also isolated from the above cDNA library. The analysis indicated the product protein, APP,was phosphorylated after its maturation. (4)There exist adenosine A_1 and A_<2B> receptors in the electric organ synaptic membrane. Activation of the latter increses the ACh release via potentiation of P/Q-type VDCCs while the activation of the former reduces the ACh release via inhibition of N-type VDCCs. (5)Antibodies from the lambert-Eaton syndrome (LES) patients reduced the ACh release by its specific down-regulation of P/Q-type VDCCs. (6)Immunization of rats or mice with the electric organ synaptosomes produced an animal model of LES.