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代谢型谷氨酸受体激活在海马CA1区去极化诱导的抑制性抑制诱导中的证据。

Evidence for metabotropic glutamate receptor activation in the induction of depolarization-induced suppression of inhibition in hippocampal CA1.

作者信息

Morishita W, Kirov S A, Alger B E

机构信息

Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

出版信息

J Neurosci. 1998 Jul 1;18(13):4870-82. doi: 10.1523/JNEUROSCI.18-13-04870.1998.

DOI:10.1523/JNEUROSCI.18-13-04870.1998
PMID:9634553
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6792551/
Abstract

Depolarization-induced suppression of inhibition (DSI) is a transient reduction of GABAA receptor-mediated IPSCs that is mediated by a retrograde signal from principal cells to interneurons. Using whole-cell recordings, we tested the hypothesis that mGluRs are involved in the DSI process in hippocampal CA1, as has been proposed for cerebellar DSI. Group II mGluR agonists failed to affect either evoked monosynaptic IPSCs or DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, but only group I agonists occluded DSI. (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduced DSI, whereas group III antagonists had no effect on DSI. Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found. Our data suggest that a glutamate-like substance released from pyramidal cells could mediate CA1 DSI by reducing GABA release from interneurons via the activation of group I mGluRs.

摘要

去极化诱导的抑制(DSI)是GABAA受体介导的抑制性突触后电流(IPSCs)的短暂减少,它由从主细胞到中间神经元的逆行信号介导。我们使用全细胞膜片钳记录技术,检验了如下假设:如小脑DSI所提出的那样,代谢型谷氨酸受体(mGluRs)参与海马CA1区的DSI过程。II组mGluR激动剂未能影响诱发的单突触IPSCs或DSI,而阻断小脑DSI的福斯高林对CA1区DSI没有影响。I组和III组mGluR激动剂可减少IPSCs,但只有I组激动剂能阻断DSI。(S)-α-甲基-4-羧基苯甘氨酸(MCPG)阻断了(1S,3R)-氨基环丙烷二羧酸(ACPD)诱导的IPSC抑制,并显著降低了DSI,而III组拮抗剂对DSI没有影响。我们还发现了DSI与(1S,3R)-ACPD诱导的IPSCs抑制之间的许多其他相似之处。我们的数据表明,从锥体细胞释放的一种谷氨酸样物质可能通过激活I组mGluRs减少中间神经元释放GABA来介导CA1区的DSI。

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