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Physiological studies on the mechanisms of synaptic transmission.

突触传递机制的生理学研究。

基本信息

批准号：
07308054
负责人：
KUBA Kenji
金额：
$ 10.75万
依托单位：
Nagoya University (1996)佐賀医科大学 (1995)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (A)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

项目摘要

This research project was organized to promote the understanding of the mechanism of synaptic transmission and composed of 14 physiologists studying synaptic transmission mechanism. New findings were presented and extensively discussed in the meetings held once a year term, leading to the new aspect of understanding of the mechanisms of synaptic transmission. The principal new findings obtained are as follows.(1) The types of Ca^<2+> channels involved in the exocytosis of neurotransmitters in various types of neurons were identified. The evidence for the role of high Ca^<2+> concentration in Ca^<2+> channel domain in exocytosis was shown. Such a high Ca^<2+> was removed by not only Na/Ca exchange and Ca pumps, but also a new unknown fast process.(2) The subunit structures of glutamate ionotropic receptors, their distributions and contributions to the generation of postsynaptic potentials and long-term synaptic plasticities, and their developmental changes were clarifiled in hippocampal and cerebellar neurons.(3) The mechanisms of interactions between G-proteins and metabotropic receptors and between G-proteins and kinases and ion channels and the involvement of these interactions in presynaptic enhancement and inhibitions were demonstrated in various types of neurons.(4) The evidence for some roles of glial cells in synaptic transmission was presented. A new gene involved in the development of synapses was cloned.

本研究项目由14位研究突触传递机制的生理学家组成，旨在促进对突触传递机制的理解。在每年一次的会议上提出了新的发现并进行了广泛的讨论，导致对突触传递机制的新认识。获得的主要新发现如下。(1)在各种类型的神经元中，参与神经递质胞吐的Ca^<2+>通道的类型被确定。这为胞吐作用中Ca^<2+>通道域的高Ca^<2 +>浓度的作用提供了证据。如此高的Ca^<2+>不仅通过Na/Ca交换和Ca泵被去除，而且还通过一种新的未知的快速过程被去除。(2)本文阐明了谷氨酸离子型受体的亚单位结构、在海马和小脑神经元中的分布、对突触后电位和长时程突触可塑性的作用及其发育变化。(3)G蛋白和代谢型受体之间以及G蛋白和激酶和离子通道之间的相互作用机制以及这些相互作用在突触前增强和抑制中的参与在各种类型的神经元中得到证实。(4)提出了胶质细胞在突触传递中的某些作用的证据。克隆了一个与突触发育有关的新基因。