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腺苷通过激活A1受体在大鼠海马体缺氧期间阻止GABAA介导的作用。

Adenosine by activating A1 receptors prevents GABAA-mediated actions during hypoxia in the rat hippocampus.

作者信息

Lucchi R, Latini S, de Mendonça A, Sebastião A M, Ribeiro J A

机构信息

Laboratory of Pharmacology, Gulbenkian Institute of Science, Oeiras, Portugal.

出版信息

Brain Res. 1996 Sep 2;732(1-2):261-6. doi: 10.1016/0006-8993(96)00748-2.

DOI:10.1016/0006-8993(96)00748-2
PMID:8891295
Abstract

The relative contribution of adenosine and gamma-aminobutyric acid (GABA) for the hypoxia-induced depression of field excitatory postsynaptic potentials in the CA1 area of rat hippocampal slices, was investigated. It is concluded that both adenosine and GABA, by activating A1 and GABAA receptors, could be responsible for the inhibition of synaptic transmission during hypoxia, but the action of endogenous GABA becomes evident only when the adenosine A1 receptor action is precluded.

摘要

研究了腺苷和γ-氨基丁酸(GABA)对大鼠海马切片CA1区缺氧诱导的场兴奋性突触后电位抑制的相对贡献。得出的结论是,腺苷和GABA通过激活A1和GABAA受体,可能在缺氧期间负责抑制突触传递,但仅当腺苷A1受体的作用被排除时,内源性GABA的作用才变得明显。

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