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丘脑网络中依赖三磷酸腺苷的亚慢波(<0.1赫兹)振荡。

ATP-dependent infra-slow (<0.1 Hz) oscillations in thalamic networks.

作者信息

Lörincz Magor L, Geall Freya, Bao Ying, Crunelli Vincenzo, Hughes Stuart W

机构信息

School of Biosciences, Cardiff University, Cardiff, UK.

出版信息

PLoS One. 2009;4(2):e4447. doi: 10.1371/journal.pone.0004447. Epub 2009 Feb 12.

Abstract

An increasing number of EEG and resting state fMRI studies in both humans and animals indicate that spontaneous low frequency fluctuations in cerebral activity at <0.1 Hz (infra-slow oscillations, ISOs) represent a fundamental component of brain functioning, being known to correlate with faster neuronal ensemble oscillations, regulate behavioural performance and influence seizure susceptibility. Although these oscillations have been commonly indicated to involve the thalamus their basic cellular mechanisms remain poorly understood. Here we show that various nuclei in the dorsal thalamus in vitro can express a robust ISO at approximately 0.005-0.1 Hz that is greatly facilitated by activating metabotropic glutamate receptors (mGluRs) and/or Ach receptors (AchRs). This ISO is a neuronal population phenomenon which modulates faster gap junction (GJ)-dependent network oscillations, and can underlie epileptic activity when AchRs or mGluRs are stimulated excessively. In individual thalamocortical neurons the ISO is primarily shaped by rhythmic, long-lasting hyperpolarizing potentials which reflect the activation of A1 receptors, by ATP-derived adenosine, and subsequent opening of Ba(2+)-sensitive K(+) channels. We argue that this ISO has a likely non-neuronal origin and may contribute to shaping ISOs in the intact brain.

摘要

越来越多针对人类和动物的脑电图及静息态功能磁共振成像研究表明,大脑活动中<0.1 Hz的自发性低频波动(超慢振荡,ISOs)是脑功能的一个基本组成部分,已知其与更快的神经元集合振荡相关,调节行为表现并影响癫痫易感性。尽管这些振荡通常被认为与丘脑有关,但其基本细胞机制仍知之甚少。在此我们表明,体外实验中背侧丘脑的各种核团能够表达一种频率约为0.005 - 0.1 Hz的强烈超慢振荡,激活代谢型谷氨酸受体(mGluRs)和/或乙酰胆碱受体(AchRs)可极大地促进这种振荡。这种超慢振荡是一种神经元群体现象,可调节更快的依赖缝隙连接(GJ)的网络振荡,当AchRs或mGluRs受到过度刺激时,它可能成为癫痫活动的基础。在单个丘脑皮质神经元中,超慢振荡主要由有节律的、持久的超极化电位形成,这些电位反映了A1受体的激活、ATP衍生的腺苷以及随后Ba(2+)敏感钾通道的开放。我们认为这种超慢振荡可能起源于非神经元,并可能有助于在完整大脑中形成超慢振荡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ab4/2637539/510190480e5a/pone.0004447.g001.jpg

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