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γ-氨基丁酸(GABA)可诱导培养的大鼠海马神经元中钙离子浓度([Ca]i)独特升高。

GABA induces a unique rise of [Ca]i in cultured rat hippocampal neurons.

作者信息

Segal M

机构信息

Department of Neurobiology, Weizmann Institute, Rehovot, Israel.

出版信息

Hippocampus. 1993 Apr;3(2):229-38. doi: 10.1002/hipo.450030214.

Abstract

GABA evoked a reversible rise of free intracellular calcium concentration ([Ca]i) in cultured rat hippocampal neurons, detected with Fluo-3 fluorescence in a confocal laser scanning microscope. The GABA-evoked change of [Ca]i was mimicked by muscimol and not by baclofen, but was only minimally affected by picrotoxin or bicuculline, indicating that this effect of GABA is not likely to be mediated by activation of GABAB receptor or by a conventional chloride-linked GABAA receptor. GABA-evoked rise of [Ca]i expressed a marked desensitization; only 10-20 minutes after a previous exposure to GABA was the response to a subsequent application fully expressed. This desensitization was not seen in electrophysiological responses to GABA or in [Ca]i changes evoked by NMDA in the same neurons. The GABA response appeared to be developmentally regulated and was seen in 1-7-day-old more than in 21-28-day-old cells. It is suggested that GABA evokes a unique change of [Ca]i in young hippocampal neurons.

摘要

在共聚焦激光扫描显微镜下,利用Fluo-3荧光检测发现,γ-氨基丁酸(GABA)可引起培养的大鼠海马神经元细胞内游离钙浓度([Ca]i)可逆性升高。蝇蕈醇可模拟GABA引起的[Ca]i变化,而巴氯芬则不能,且GABA的这种效应仅受到轻微的印防己毒素或荷包牡丹碱影响,这表明GABA的这种效应不太可能是由GABAB受体激活或传统的氯离子连接GABAA受体介导的。GABA引起的[Ca]i升高表现出明显的脱敏现象;在前一次暴露于GABA后仅10 - 20分钟,对随后再次应用GABA的反应才会充分表现出来。在相同神经元中,这种脱敏现象在对GABA的电生理反应或N-甲基-D-天冬氨酸(NMDA)引起的[Ca]i变化中并未出现。GABA反应似乎受到发育调控,在1 - 7日龄的细胞中比在21 - 28日龄的细胞中更明显。研究表明,GABA在年轻的海马神经元中引起独特的[Ca]i变化。

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