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电生性钠钾泵在培养的脊髓神经网络去抑制诱导爆发中的作用。

Role of the electrogenic Na/K pump in disinhibition-induced bursting in cultured spinal networks.

作者信息

Darbon P, Tscherter A, Yvon C, Streit J

机构信息

Institute of Physiology, University of Bern, 3012 Bern, Switzerland.

出版信息

J Neurophysiol. 2003 Nov;90(5):3119-29. doi: 10.1152/jn.00579.2003. Epub 2003 Jul 30.

DOI:10.1152/jn.00579.2003
PMID:12890799
Abstract

Disinhibition-induced bursting activity in cultures of fetal rat spinal cord is mainly controlled by intrinsic spiking with subsequent recurrent excitation of the network through glutamate synaptic transmission, and by autoregulation of neuronal excitability. Here we investigated the contribution of the electrogenic Na/K pump to the autoregulation of excitability using extracellular recordings by multielectrode arrays (MEAs) and intracellular whole cell recordings from spinal interneurons. The blockade of the electrogenic Na/K pump by strophanthidin led to an immediate and transient increase in the burst rate together with an increase in the asynchronous background activity. Later, the burst rate decreased to initial values and the bursts became shorter and smaller. In single neurons, we observed an immediate depolarization of the membrane during the interburst intervals concomitant with the rise in burst rate. This depolarization was more pronounced during disinhibition than during control, suggesting that the pump was more active. Later a decrease in burst rate was observed and, in some neurons, a complete cessation of firing. Most of the effects of strophanthidin could be reproduced by high K+-induced depolarization. During prolonged current injections, spinal interneurons exhibited spike frequency adaptation, which remained unaffected by strophanthidin. These results suggest that the electrogenic Na/K pump is responsible for the hyperpolarization and thus for the changes in excitability during the interburst intervals, although not for the spike frequency adaptation during the bursts.

摘要

胎鼠脊髓培养物中去抑制诱导的爆发活动主要受内在发放控制,随后通过谷氨酸突触传递对网络进行反复兴奋,并受神经元兴奋性的自动调节。在这里,我们使用多电极阵列(MEA)进行细胞外记录以及对脊髓中间神经元进行细胞内全细胞记录,研究了电生钠钾泵对兴奋性自动调节的作用。毒毛花苷对电生钠钾泵的阻断导致爆发频率立即短暂增加,同时异步背景活动增加。随后,爆发频率降至初始值,且爆发变得更短、更小。在单个神经元中,我们观察到在爆发间隔期间膜立即去极化,同时爆发频率上升。这种去极化在去抑制期间比在对照期间更明显,表明泵更活跃。随后观察到爆发频率降低,并且在一些神经元中,放电完全停止。毒毛花苷的大多数作用可通过高钾诱导的去极化来重现。在长时间电流注入期间,脊髓中间神经元表现出动作电位频率适应性,这不受毒毛花苷影响。这些结果表明,电生钠钾泵负责超极化,从而负责爆发间隔期间兴奋性的变化,尽管不负责爆发期间的动作电位频率适应性。

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