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沙土鼠海马中缺血诱导的磷脂酰肌醇-4,5-二磷酸(PIP2)水平变化。

Ischemia-induced changes in PIP2 levels of gerbil hippocampus.

作者信息

Ishida A, Shimazaki K, Kawai N

机构信息

Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.

出版信息

Neurosci Res. 1992 Dec;15(4):305-9. doi: 10.1016/0168-0102(92)90053-f.

DOI:10.1016/0168-0102(92)90053-f
PMID:1337583
Abstract

We carried out an immunohistochemical study to detect changes in phosphatidylinositol 4,5-bisphosphate (PIP2) in gerbil hippocampus at various times after transient ischemia, using an anti-PIP2 antibody. About 24 h after transient ischemia for 5 min, an increase in the immunoreactivity was observed which was restricted to the area of CA1 pyramidal neurons. On the other hand, after less severe ischemia lasting 2 min, which did not lead to neuronal death, a decrease in PIP2 immunoreactivity was observed at about 48 h. The results indicate that levels of PIP2 following ischemia reflect dynamic changes in phosphatidylinositol (PI) turnover which may be related to neuronal degeneration.

摘要

我们使用抗磷脂酰肌醇 - 4,5 - 二磷酸(PIP2)抗体进行了一项免疫组织化学研究,以检测沙土鼠海马体在短暂性缺血后不同时间点PIP2的变化。短暂性缺血5分钟后约24小时,观察到免疫反应性增加,且仅限于CA1锥体神经元区域。另一方面,在持续2分钟的不太严重的缺血(未导致神经元死亡)后,约48小时观察到PIP2免疫反应性降低。结果表明,缺血后PIP2水平反映了磷脂酰肌醇(PI)周转的动态变化,这可能与神经元变性有关。

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