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突触后G蛋白参与海马体长期增强效应。

Involvement of postsynaptic G-proteins in hippocampal long-term potentiation.

作者信息

Satoh M, Kaneko S

机构信息

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.

出版信息

Rev Neurosci. 1994 Jan-Mar;5(1):1-9. doi: 10.1515/revneuro.1994.5.1.1.

Abstract

The guanine nucleotide binding proteins (G-proteins) are a family of proteins that couple membrane receptors to intracellular second messenger enzymes. Most subtypes of G-protein are highly expressed in hippocampal neurons, implying important roles of G-proteins in the modulation of synaptic transmission. In this article, we review recent studies on the involvement of G-proteins in tetanus-induced long-term potentiation (LTP) of synaptic efficacy in the hippocampus. Such an LTP has been demonstrated to be produced by several mechanisms. In Schaffer collateral-CA1 synapses where induction of LTP requires post- and presynaptic events, G-proteins may regulate the development of LTP presynaptically. In mossy fiber-CA3 synapses where only presynaptic elements are needed to initiate LTP, the contribution of G-proteins may also be localized at presynaptic sites. However, in fimbria-CA3 synapses where LTP is thought to be initiated by NMDA receptor activation at CA1 pyramidal cells, postsynaptic G-proteins are involved in the induction of LTP by affecting membrane depolarization and/or Ca2+ mobilization. The different contribution of G-proteins in the various forms of LTP at anatomically distinct synapses implies localized modification of synaptic transmission by endogenous neurotransmitters via G-protein-coupled receptors.

摘要

鸟嘌呤核苷酸结合蛋白(G蛋白)是一类将膜受体与细胞内第二信使酶偶联的蛋白质。大多数G蛋白亚型在海马神经元中高度表达,这意味着G蛋白在调节突触传递中具有重要作用。在本文中,我们综述了关于G蛋白参与海马体中破伤风诱导的突触效能长期增强(LTP)的最新研究。这种LTP已被证明是由多种机制产生的。在LTP诱导需要突触后和突触前事件的海马体Schaffer侧支-CA1突触中,G蛋白可能在突触前调节LTP的发展。在仅需要突触前元件来启动LTP的苔藓纤维-CA3突触中,G蛋白的作用也可能定位于突触前部位。然而,在认为LTP由CA1锥体细胞处的NMDA受体激活引发的海马伞-CA3突触中,突触后G蛋白通过影响膜去极化和/或Ca2+动员参与LTP的诱导。G蛋白在解剖学上不同的突触处的各种形式的LTP中的不同作用意味着内源性神经递质通过G蛋白偶联受体对突触传递进行局部修饰。

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