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抑制大鼠海马脑片N-甲基-D-天冬氨酸诱导的短期增强效应。

Inhibition of an N-methyl-D-aspartate induced short-term potentiation in the rat hippocampal slice.

作者信息

McGuinness N, Anwyl R, Rowan M

机构信息

Department of Physiology, Trinity College, Dublin, Ireland.

出版信息

Brain Res. 1991 Oct 25;562(2):335-8. doi: 10.1016/0006-8993(91)90643-a.

Abstract

The effects of the phorbol ester 4 beta-phorbol-12,13 dibutyrate (PDBu) and the protein kinase (PK) inhibitors H-7 and sphingosine were investigated on the short-term potentiation (STP) of the population excitatory postsynaptic potential (EPSP) induced by perfusion of N-methyl-D-aspartate (NMDA) in the stratum radiatum of CA1 of the rat hippocampal slice. Bath perfusion of 130 microM NMDA for 10 s caused an initial depression of the population EPSP followed by a STP, which averaged 46% and lasted 16 min. PDBu (100 nM) perfused for 2 h completely inhibited the NMDA induced STP, suggesting that the stimulation of PKC inhibited an NMDA receptor activated process which induced the STP. The protein kinase inhibitors H-7 and sphingosine did not alter the NMDA induced STP.

摘要

研究了佛波酯4β-佛波醇-12,13-二丁酸酯(PDBu)以及蛋白激酶(PK)抑制剂H-7和鞘氨醇对大鼠海马切片CA1区辐射层中通过灌注N-甲基-D-天冬氨酸(NMDA)诱导的群体兴奋性突触后电位(EPSP)的短期增强(STP)的影响。用130微摩尔/升的NMDA进行10秒的浴槽灌注会导致群体EPSP先出现抑制,随后出现短期增强,平均增强46%,持续16分钟。灌注100纳摩尔/升的PDBu 2小时可完全抑制NMDA诱导的短期增强,这表明蛋白激酶C的激活抑制了诱导短期增强的NMDA受体激活过程。蛋白激酶抑制剂H-7和鞘氨醇并未改变NMDA诱导的短期增强。

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