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癫痫持续状态后大鼠海马小白蛋白阳性神经元内P/Q型电压门控性Ca2+通道免疫反应性上调。

Up-regulation of P/Q-type voltage-gated Ca2+ channel immunoreactivity within parvalbumin positive neurons in the rat hippocampus following status epilepticus.

作者信息

Kim Ji-Eun, Kwak Sung-Eun, Kim Duk-Soo, Won Moo Ho, Choi Hui-Chul, Song Hong-Ki, Kim Yeong-In, Kang Tae-Cheon

机构信息

Department of Anatomy, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.

出版信息

Neurosci Res. 2007 Mar;57(3):379-86. doi: 10.1016/j.neures.2006.11.007. Epub 2006 Dec 11.

Abstract

To identify the roles of VGCC subtypes in damages/impairs of inhibitory transmission during epileptogenesis, we investigated temporal- and spatial-specific alterations in voltage-gated Ca(2+) channel (VGCC) immunoreactivities within parvalbumin (PV, a Ca(2+) binding protein) positive neurons in the rat hippocampus following status epilepticus (SE). Compared to controls, only P/Q-type (alpha1A) VGCC immunoreactivity was enhanced in PV positive neurons at the early point following SE. The alteration in P/Q-type (alpha1A) VGCC immunoreactivity showed an inverse proportionality to that in PV immunoreactivity in the dentate gyrus and the CA1 region. These findings suggest that SE may induce prolonged up-regulation in P/Q-type VGCC expression within PV positive neurons.

摘要

为了确定电压门控钙通道(VGCC)亚型在癫痫发生过程中抑制性传递损伤中的作用,我们研究了癫痫持续状态(SE)后大鼠海马中帕瓦丁(PV,一种钙结合蛋白)阳性神经元内电压门控钙通道(VGCC)免疫反应性的时空特异性变化。与对照组相比,仅在SE后的早期,PV阳性神经元中的P/Q型(α1A)VGCC免疫反应性增强。齿状回和CA1区中P/Q型(α1A)VGCC免疫反应性的变化与PV免疫反应性的变化呈反比。这些发现表明,SE可能诱导PV阳性神经元内P/Q型VGCC表达的长期上调。

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