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在CA1锥体神经元的θ振荡期间,GABA(A)受体介导的抑制对峰电位时间的双向控制。

Bidirectional control of spike timing by GABA(A) receptor-mediated inhibition during theta oscillation in CA1 pyramidal neurons.

作者信息

Kwag Jeehyun, Paulsen Ole

机构信息

Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.

出版信息

Neuroreport. 2009 Aug 26;20(13):1209-13. doi: 10.1097/WNR.0b013e32832f5cc7.

DOI:10.1097/WNR.0b013e32832f5cc7
PMID:19617859
Abstract

Precisely controlled spike times relative to theta-frequency network oscillations play an important role in hippocampal memory processing. Here we study how inhibitory synaptic input during theta oscillation contributes to the control of spike timing. Using whole-cell patch-clamp recordings from CA1 pyramidal cells in vitro with dynamic clamp to simulate theta-frequency oscillation (5 Hz), we show that gamma-aminobutyric acid-A (GABA(A)) receptor-mediated inhibitory postsynaptic potentials (IPSPs) can not only delay but also advance the postsynaptic spike depending on the timing of the inhibition relative to the oscillation. Spike time advancement with IPSP was abolished by the h-channel blocker ZD7288 (10 microM), suggesting that IPSPs can interact with intrinsic membrane conductances to yield bidirectional control of spike timing.

摘要

相对于theta频率网络振荡的精确控制的尖峰时间在海马体记忆处理中起着重要作用。在这里,我们研究theta振荡期间的抑制性突触输入如何有助于控制尖峰时间。使用体外CA1锥体细胞的全细胞膜片钳记录并结合动态钳来模拟theta频率振荡(5赫兹),我们发现γ-氨基丁酸-A(GABA(A))受体介导的抑制性突触后电位(IPSPs)不仅可以延迟,还可以根据抑制相对于振荡的时间提前突触后尖峰。h通道阻滞剂ZD7288(10微摩尔)消除了IPSP引起的尖峰时间提前,这表明IPSPs可以与内在膜电导相互作用,从而对尖峰时间产生双向控制。

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