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海马体CA1区腔隙-分子层中间神经元。II. 局部回路突触相互作用的胞体和树突内记录。

Stratum lacunosum-moleculare interneurons of hippocampal CA1 region. II. Intrasomatic and intradendritic recordings of local circuit synaptic interactions.

作者信息

Lacaille J C, Schwartzkroin P A

机构信息

Department of Neurological Surgery, University of Washington, Seattle 98195.

出版信息

J Neurosci. 1988 Apr;8(4):1411-24. doi: 10.1523/JNEUROSCI.08-04-01411.1988.

DOI:10.1523/JNEUROSCI.08-04-01411.1988
PMID:3357024
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6569260/
Abstract

Simultaneous intracellular recordings were obtained from stratum lacunosum-moleculare (L-M) interneurons and CA1 cells, and their local circuit synaptic interactions were examined. Synaptic interactions with pyramidal cells were evaluated in both intrasomatic and intradendritic pyramidal cell recordings. Stimulation of L-M interneurons evoked small-amplitude IPSPs in 21% of intrasomatic (9/42 cell pairs) and in 26% of intradendritic (11/43) pyramidal cell recordings. The IPSP mean peak amplitude was 0.91 mV for intrasomatic and 0.67 mV for intradendritic recordings. IPSPs had slow onset and decay (approximately 80-90 msec), decreased in amplitude with membrane hyperpolarization, and were not associated with any apparent change in input resistance. No physiologic evidence of synaptic connections was found from pyramidal cells to L-M interneurons. Inhibitory synaptic interactions were also seen between L-M interneurons and stratum pyramidale interneurons (2 of 4 cell pairs). The IPSPs recorded in pyramidale interneurons were similar to the IPSPs recorded in pyramidal cells. During simultaneous recordings, L-M interneurons were activated at a shorter latency, i.e., in a feedforward manner with respect to pyramidal cells. Thus, L-M interneurons may mediate feedforward inhibition of CA1 pyramidal cells. The L-M interneuron-evoked IPSPs in pyramidal cells share some characteristics of the late IPSP recorded in CA1 pyramidal cells and may therefore contribute to this component of the IPSP.

摘要

同时从海马分子层-腔隙层(L-M)中间神经元和CA1细胞进行细胞内记录,并检测它们的局部回路突触相互作用。在体细胞内和树突内的锥体细胞记录中评估与锥体细胞的突触相互作用。刺激L-M中间神经元在21%的体细胞内记录(9/42对细胞)和26%的树突内记录(11/43)的锥体细胞中诱发小幅度抑制性突触后电位(IPSP)。体细胞内记录的IPSP平均峰值幅度为0.91 mV,树突内记录为0.67 mV。IPSP起始和衰减缓慢(约80 - 90毫秒),随着膜超极化幅度减小,且与输入电阻的任何明显变化无关。未发现从锥体细胞到L-M中间神经元有突触连接的生理学证据。在L-M中间神经元和锥体层中间神经元之间也观察到抑制性突触相互作用(4对细胞中的2对)。在锥体层中间神经元记录的IPSP与在锥体细胞中记录的IPSP相似。在同时记录期间,L-M中间神经元以较短的潜伏期被激活,即相对于锥体细胞以前馈方式激活。因此,L-M中间神经元可能介导对CA1锥体细胞的前馈抑制。L-M中间神经元在锥体细胞中诱发的IPSP具有在CA1锥体细胞中记录的晚期IPSP的一些特征,因此可能对IPSP的这一成分有贡献。