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突触后Ca2+的螯合作用促进海马体抑制性突触后电位的长期增强。

Chelation of postsynaptic Ca2+ facilitates long-term potentiation of hippocampal IPSPs.

作者信息

Morishita W, Sastry B R

机构信息

Department of Pharmacology and Therapeutics, University of British Columbia, Vancouver, Canada.

出版信息

Neuroreport. 1991 Sep;2(9):533-6. doi: 10.1097/00001756-199109000-00009.

Abstract

In guinea pig hippocampal slices, a tetanic stimulation of the stratum radiatum caused long-term potentiation (LTP) of the excitatory postsynaptic potential (EPSP) but not of the GABAB receptor-mediated slow inhibitory postsynaptic potential (IPSP) in the CA1 neurons. In neurons in which Ca2+ was chelated with 1,2-bis(2-aminophenoxy) ethane N,N,N',N'-tetra-acetic acid (BAPTA) or ethylene-bis(oxyethylenenitrilo)tetra-acetic acid (EGTA), tetanic stimulation of the stratum radiatum caused LTP of the slow IPSP but not of the EPSP. These results indicate that a reciprocal relationship exists between LTP of the EPSP and LTP of the slow IPSP as far as the involvement of the postsynaptic Ca2+ is concerned.

摘要

在豚鼠海马切片中,对辐射层进行强直刺激可引起CA1神经元兴奋性突触后电位(EPSP)的长时程增强(LTP),但不会引起GABAB受体介导的慢抑制性突触后电位(IPSP)的LTP。在使用1,2-双(2-氨基苯氧基)乙烷-N,N,N',N'-四乙酸(BAPTA)或乙二醇双(氧乙烯腈)四乙酸(EGTA)螯合Ca2+的神经元中,对辐射层进行强直刺激可引起慢IPSP的LTP,但不会引起EPSP的LTP。这些结果表明,就突触后Ca2+的参与而言,EPSP的LTP与慢IPSP的LTP之间存在相互关系。

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