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在大鼠CA1神经元中,格列本脲可抑制腺苷诱导的超极化。

Adenosine-induced hyperpolarization is depressed by glibenclamide in rat CA1 neurones.

作者信息

Li H, Henry J L

机构信息

Department of Psychiatry, McGill University, Montreal, Quebec, Canada.

出版信息

Neuroreport. 1992 Dec;3(12):1113-6. doi: 10.1097/00001756-199212000-00020.

DOI:10.1097/00001756-199212000-00020
PMID:1493225
Abstract

The effect of the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel blocker, glibenclamide, on adenosine-induced postsynaptic hyperpolarization was studied by means of intracellular recording techniques in TTX-treated CA1 neurones in the rat hippocampal slice. Glibenclamide applied in the CSF perfusion fluid at 30 microM reversibly depressed the 2-chloroadenosine-induced hyperpolarization and the increase in the membrane conductance. It is suggested that adenosine induces the opening of potassium channels in the postsynaptic membrane of CA1 neurones, including KATP channels in the mammalian central nervous system (CNS).

摘要

采用细胞内记录技术,在经河豚毒素(TTX)处理的大鼠海马切片CA1神经元中,研究了三磷酸腺苷(ATP)敏感性钾(KATP)通道阻断剂格列本脲对腺苷诱导的突触后超极化的影响。在脑脊液灌注液中加入30微摩尔的格列本脲,可可逆性地抑制2-氯腺苷诱导的超极化和膜电导增加。提示腺苷可诱导CA1神经元突触后膜钾通道开放,包括哺乳动物中枢神经系统(CNS)中的KATP通道。

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