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中间神经元上兴奋性突触的短暂抑制导致小鼠海马切片γ振荡期间的癫痫样爆发。

Transient depression of excitatory synapses on interneurons contributes to epileptiform bursts during gamma oscillations in the mouse hippocampal slice.

作者信息

Traub Roger D, Pais Isabel, Bibbig Andrea, Lebeau Fiona E N, Buhl Eberhard H, Garner Helen, Monyer Hannah, Whittington Miles A

机构信息

Departments of Physiology and Pharmacology, and Neurology, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA.

出版信息

J Neurophysiol. 2005 Aug;94(2):1225-35. doi: 10.1152/jn.00069.2005. Epub 2005 Feb 23.

DOI:10.1152/jn.00069.2005
PMID:15728773
Abstract

Persistent gamma frequency (30-70 Hz) network oscillations occur in hippocampal slices under conditions of metabotropic glutamate receptor (mGluR) activation. Excessive mGluR activation generated a bistable pattern of network activity during which epochs of gamma oscillations of increasing amplitude were terminated by synchronized bursts and very fast oscillations (>70 Hz). We provide experimental evidence that, during this behavior, pyramidal cell-to-interneuron synaptic depression takes place, occurring spontaneously during the gamma rhythm and associated with the onset of epileptiform bursts. We further provide evidence that excitatory postsynaptic potentials (EPSPs) in pyramidal cells are potentiated during the interburst gamma oscillation. When these two types of synaptic plasticity are incorporated, phenomenologically, into a network model previously shown to account for many features of persistent gamma oscillations, we find that epochs of gamma do indeed alternate with epochs of very fast oscillations and epileptiform bursts. Thus the same neuronal network can generate either gamma oscillations or epileptiform bursts, in a manner depending on the degree of network drive and network-induced fluctuations in synaptic efficacies.

摘要

在代谢型谷氨酸受体(mGluR)激活的条件下,海马切片中会出现持续的γ频率(30 - 70赫兹)网络振荡。过度的mGluR激活会产生一种双稳态的网络活动模式,在此期间,振幅不断增加的γ振荡会被同步爆发和极快速振荡(>70赫兹)终止。我们提供了实验证据表明,在此行为过程中,锥体细胞到中间神经元的突触会发生抑制,在γ节律期间自发出现,并与癫痫样爆发的起始相关。我们还进一步证明,在爆发间期的γ振荡期间,锥体细胞中的兴奋性突触后电位(EPSP)会增强。当从现象学角度将这两种类型的突触可塑性纳入一个先前已被证明能解释持续γ振荡许多特征的网络模型时,我们发现γ振荡期确实会与极快速振荡期和癫痫样爆发期交替出现。因此,同一神经网络可以根据网络驱动程度和网络诱导的突触效能波动,以不同方式产生γ振荡或癫痫样爆发。

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