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雪貂膝周神经元体外慢后超极化的功能和离子特性

Functional and ionic properties of a slow afterhyperpolarization in ferret perigeniculate neurons in vitro.

作者信息

Kim U, McCormick D A

机构信息

Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.

出版信息

J Neurophysiol. 1998 Sep;80(3):1222-35. doi: 10.1152/jn.1998.80.3.1222.

DOI:10.1152/jn.1998.80.3.1222
PMID:9744934
Abstract

Intracellular recordings from spontaneously spindling GABAergic neurons of the ferret perigeniculate nucleus in vitro revealed a fast afterhyperpolarization after each action potential, a medium-duration afterhyperpolarization after each low-threshold Ca2+ spike, and a slow afterhyperpolarization after the cessation of spindle waves. The slow afterhyperpolarization was associated with an increase in membrane conductance, and the reversal potential was sensitive to extracellular [K+]o, indicating that it is mediated at least in part by the activation of a K+ conductance. However, the block of Ca2+ channels did not block the slow afterhyperpolarization, whereas the block of Na+ channels did block this event, even after the generation of repetitive Ca2+ spikes, indicating that it is mediated by a Na+-activated K+ current. Application of apamin reduced the afterhyperpolarization and enhanced a plateau potential after each low-threshold Ca2+ spike. This plateau potential could result in a prolonged depolarization of perigeniculate neurons, even before the application of apamin, resulting in the generation of tonic discharge. The plateau potential was blocked by the local application of tetrodotoxin, indicating that it is mediated by a persistent Na+ current. The activation and interaction of these slowly developing and persistent currents contributes significantly to low-frequency components of spindle wave generation. In particular, we suggest that the activation of the slow afterhyperpolarization may contribute to the generation of the spindle wave refractory period in vitro.

摘要

对雪貂外侧膝状体核体外自发产生纺锤波的GABA能神经元进行细胞内记录发现,每个动作电位后出现快速超极化后电位,每个低阈值Ca2+ 峰电位后出现中等时程的超极化后电位,纺锤波停止后出现缓慢超极化后电位。缓慢超极化后电位与膜电导增加有关,其反转电位对细胞外[K+]o敏感,表明它至少部分由K+ 电导的激活介导。然而,Ca2+ 通道的阻断并未阻断缓慢超极化后电位,而Na+ 通道的阻断则阻断了该事件,即使在产生重复性Ca2+ 峰电位后也是如此,这表明它由Na+ 激活的K+ 电流介导。应用蜂毒明肽可减少超极化后电位,并增强每个低阈值Ca2+ 峰电位后的平台电位。即使在应用蜂毒明肽之前,这种平台电位也可能导致外侧膝状体神经元的去极化延长,从而导致强直放电的产生。平台电位可被局部应用河豚毒素阻断,表明它由持续性Na+ 电流介导。这些缓慢发展和持续的电流的激活和相互作用对纺锤波产生的低频成分有显著贡献。特别是,我们认为缓慢超极化后电位的激活可能有助于体外纺锤波不应期的产生。

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