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黑质内γ-乙烯基-GABA的抗惊厥作用:去甲肾上腺素能神经传递的作用

Anticonvulsant action of intranigral gamma-vinyl-GABA: role of nonadrenergic neurotransmission.

作者信息

Bonhaus D W, McNamara J O

机构信息

Department of Medicine (Neurology), Duke University Medical Center, Durham, NC.

出版信息

Brain Res. 1988 Jan 12;438(1-2):391-4. doi: 10.1016/0006-8993(88)91370-4.

Abstract

Intranigral gamma-vinyl-GABA (GVG) suppresses electroshock seizures (ES). This anticonvulsant action was blocked by systemic treatment with the alpha 2-antagonist idazoxan. Consequently, we tested the idea that intranigral GABA mimetics suppress ES by increasing noradrenergic (NE) neuronal activity. Contrary to our hypothesis, GVG decreased NE turnover. This result indicates that while the seizure-suppressant effect of intranigral GVG requires alpha 2-mediated NE neurotransmission, the mechanism of this anticonvulsant action is not by increasing NE neuronal activity.

摘要

脑内注射γ-乙烯基-GABA(GVG)可抑制电休克惊厥(ES)。这种抗惊厥作用可被α2拮抗剂伊达唑胺的全身治疗所阻断。因此,我们测试了脑内注射GABA模拟物通过增加去甲肾上腺素能(NE)神经元活动来抑制ES的想法。与我们的假设相反,GVG降低了NE的更新率。这一结果表明,虽然脑内注射GVG的抗惊厥作用需要α2介导的NE神经传递,但其抗惊厥作用机制并非通过增加NE神经元活动。

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