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Electrophysiological studies of synaptic transmission in the central and peripheral autonomic neurons.

中枢和外周自主神经元突触传递的电生理学研究。

基本信息

批准号：
03454134
负责人：
NISHI Syogoro
金额：
$ 4.16万
依托单位：
Kurume University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-03454134/
关键词：
sympathetic preganglionic neuron fast EPSP presynaptic inhibition alpha_1 and alpha_2 receptor slow EPSP and IPSP signal transduction serotonin tachykinin 緩徐シナプス電位ノルアドレナリン substance P alpha_1受容体 alpha_2受容体シグナル・トランスダクション slow

项目摘要

1. Presynaptic regulation of sympathetic preganglionic neurons (SPN) : Noradrenaline (NA) inhibits the fast EPSP presynaptically This inhibiton appeared to be due to activation of alpha_2 receptors on the gultaminergic presynaptic nerve terminals that might cause hyperpolarization and/or reduction of Ca conductance of the terminal membrane.2. The receptor and signal transduction mechanisms underlying the catecholaminergic transmission in SPNs : The alpha_1 and alpha_2 receptors on SPNs, respectively, mediate the slow EPSP and the slow IPSP.The alpha_1 receptors are endowed mainly on the dendrites and the alpha_2 receptors on the soma. The former produces the slow response via G-protein and proteinkinase C and the latter via G-protein alone.3. The indolaminergic and peptidergic transmissions in SPNs : Both serotonin (5-HT) and tachykinins cause reduction of the Ca-dependent K conductance that results in a slow depolarization and the inhibition of the slow afterhyperpolarization of SPNs. The 5-HT action is mediated by 5-HT_2 receptors.4. Intracellular signal transduction that mediates the slow IPSP in submucous neurons of the guinea-pig caecum : The mechanisms underlying intracellular signal transduction of the slow IPSP mediated by NA appeared to be following : i) the increased K conductance was mediated by the activation of pertussis toxin-sensitive G protein and the corresponding accumulation of intracellular Ca^<2+> released from the internal stores by IP_3. The binding of the released Ca^<2+> to calmoduline might result in an increase in potassium conductance.

1. 交感神经节前神经元（SPN）的突触前调控：去甲肾上腺素（NA）抑制快速EPSP的突触前调控，这种抑制可能是由于谷胺能突触前神经末梢α _2受体的激活，可能导致末梢膜的超极化和/或Ca电导降低。spn中儿茶酚胺能传递的受体和信号转导机制：spn上的alpha_1和alpha_2受体分别介导慢速EPSP和慢速IPSP。α _1受体主要分布在树突上，α _2受体主要分布在体细胞上。前者通过g蛋白和蛋白激酶C产生缓慢反应，后者仅通过g蛋白产生缓慢反应。spn的吲哚胺能和多肽能传递：血清素（5-HT）和速激素都能导致钙依赖性K电导的减少，从而导致spn的缓慢去极化和抑制缓慢的后超极化。5-羟色胺的作用由5-羟色胺受体介导。介导豚鼠盲肠粘膜下神经元慢IPSP的胞内信号转导：NA介导慢IPSP的胞内信号转导机制如下：1)百日咳毒素敏感G蛋白的激活和IP_3释放的细胞内Ca^<2+>的积累介导了K电导的增加。释放的Ca^<2+>与钙调素的结合可能导致钾电导的增加。