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尼莫地平可预防大鼠局灶性脑缺血后海马CA1区小白蛋白免疫反应性的早期丧失。

Nimodipine prevents early loss of hippocampal CA1 parvalbumin immunoreactivity after focal cerebral ischemia in the rat.

作者信息

Benyó Z, De Jong G I, Luiten P G

机构信息

Department of Animal Physiology, University of Groningen, The Netherlands.

出版信息

Brain Res Bull. 1995;36(6):569-72. doi: 10.1016/0361-9230(94)00246-w.

Abstract

The effect of focal cerebral ischemia induced by middle cerebral artery occlusion on hippocampal interneurons containing the calcium-binding protein parvalbumin (PV) was studied in rats. Four hours after the onset of ischemia, a reduced number of PV-immunoreactive (-ir) neurons was observed in the lateral part of the CA1 region, while PV-ir was not altered in the CA2 and CA3 areas. Pretreatment with the L-type Ca2+ channel blocker nimodipine prevented the ischemia-induced loss of PV-ir in the CA1, suggesting a role for L-type voltage sensitive calcium channels in the mechanism of early neuronal alterations in the hippocampus CA1 region after focal cerebral ischemia.

摘要

在大鼠中研究了大脑中动脉闭塞诱导的局灶性脑缺血对含有钙结合蛋白小白蛋白(PV)的海马中间神经元的影响。缺血发作后4小时,在CA1区外侧观察到PV免疫反应性(-ir)神经元数量减少,而CA2和CA3区的PV-ir没有改变。用L型Ca2+通道阻滞剂尼莫地平预处理可防止CA1区缺血诱导的PV-ir丢失,提示L型电压敏感钙通道在局灶性脑缺血后海马CA1区早期神经元改变机制中起作用。

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