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海马体中GABA能门控的异突触转变及碳酸酐酶抑制的作用

Heterosynaptic transformation of GABAergic gating in the hippocampus and effects of carbonic anhydrase inhibition.

作者信息

Sun M, Dahl D, Alkon D L

机构信息

Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

J Pharmacol Exp Ther. 2001 Mar;296(3):811-7.

Abstract

Recordings from CA1 pyramidal cells were made in rat hippocampal slices (in vitro). Activation of cholinergic receptors associated with tetanization of GABAergic inputs from stratum pyramidale transformed the hyperpolarizing GABA-mediated inhibitory postsynaptic potentials into depolarizing responses of rat hippocampal CA1 pyramidal neurons. The synaptic transformation was characterized by a significant shift of reversal potential of postsynaptic responses toward positive membrane potentials. This effect lasted more than 1 h and changed the function of the GABAergic synapses from excitation filter to amplifier. This long-term synaptic transformation was prevented by carbonic anhydrase inhibitors or the presence of HEPES buffer, indicating a dependence on HCO(3-). The presence or absence of an associated activation of cholinergic with GABAergic inputs thus gates the information processing through the pyramidal cells and network, forming an amplified "center" of attention and a filtered "surround". Information flow through the neural circuit is thereby directed according to temporal association of the relevant signals.

摘要

在大鼠海马切片(体外)中对CA1锥体细胞进行记录。与来自锥体层的GABA能输入的强直刺激相关的胆碱能受体激活,将超极化的GABA介导的抑制性突触后电位转变为大鼠海马CA1锥体神经元的去极化反应。这种突触转变的特征是突触后反应的反转电位向正膜电位显著偏移。这种效应持续超过1小时,并将GABA能突触的功能从兴奋滤波器转变为放大器。碳酸酐酶抑制剂或HEPES缓冲液的存在可阻止这种长期的突触转变,表明其对HCO₃⁻的依赖性。胆碱能与GABA能输入的相关激活的存在与否,从而控制通过锥体细胞和网络的信息处理,形成一个放大的“注意力中心”和一个过滤的“周边”。由此,通过神经回路的信息流根据相关信号的时间关联被引导。

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