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海马体长期增强效应中一种对百日咳毒素敏感的G蛋白。

A pertussis toxin-sensitive G protein in hippocampal long-term potentiation.

作者信息

Goh J W, Pennefather P S

机构信息

Faculty of Pharmacy, University of Toronto, Ontario, Canada.

出版信息

Science. 1989 May 26;244(4907):980-3. doi: 10.1126/science.2543072.

Abstract

High-frequency (tetanic) stimulation of presynaptic nerve tracts in the hippocampal region of the brain can lead to long-term synaptic potentiation (LTP). Pertussis toxin prevented the development of tetanus-induced LTP in the stratum radiatum-CA1 synaptic system of rat hippocampal slices, indicating that a guanosine triphosphate-binding protein (G protein) may be required for the initiation of LTP. This G protein may be located at a site distinct from the postsynaptic neuron (that is, in presynaptic terminals or glial cells) since maximal activation of CA1 neuronal G proteins by intracellular injection of guanosine-5'-O-(3-thiotriphosphate), a nonhydrolyzable analog of guanosine 5'-triphosphate, did not occlude LTP.

摘要

对大脑海马区的突触前神经束进行高频(强直)刺激可导致长期突触增强(LTP)。百日咳毒素可阻止大鼠海马切片辐射层-CA1突触系统中破伤风诱导的LTP的发展,这表明鸟苷三磷酸结合蛋白(G蛋白)可能是LTP起始所必需的。这种G蛋白可能位于与突触后神经元不同的位点(即突触前终末或神经胶质细胞中),因为通过细胞内注射鸟苷-5'-O-(3-硫代三磷酸)(鸟苷5'-三磷酸的一种不可水解类似物)对CA1神经元G蛋白进行最大激活并未阻断LTP。

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