大鼠脑内 kainic 酸诱导损伤后星形胶质细胞中连接蛋白 43 免疫反应性的缺失

Depletion of connexin43-immunoreactivity in astrocytes after kainic acid-induced lesions in rat brain.

作者信息

Vukelic J I, Yamamoto T, Hertzberg E L, Nagy J I

机构信息

Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

出版信息

Neurosci Lett. 1991 Sep 2;130(1):120-4. doi: 10.1016/0304-3940(91)90242-l.

DOI:10.1016/0304-3940(91)90242-l

PMID:1660969

Abstract

Recent studies have established that the gap junction protein connexin43 is a major structural component of gap junctions between astrocytes in rat brain. Here, we investigated by immunohistochemical methods the effect of kainic acid-induced neuronal degeneration on connexin43 expression by astrocytes. Stereotaxic injections of kainic acid into the thalamus were found to cause a near total depletion of connexin43-immunoreactivity at the lesion site. Areas depleted of connexin43 corresponded to those exhibiting substantial neuronal loss and intense gliosis. These results implicate a neuronal contribution to the regulation of connexin43 expression by astrocytes and, hence, to local control of the potassium spatial buffering capacity afforded by astrocyte gap junctions.

摘要

最近的研究表明，缝隙连接蛋白连接蛋白43是大鼠脑内星形胶质细胞之间缝隙连接的主要结构成分。在此，我们通过免疫组织化学方法研究了海藻酸诱导的神经元变性对星形胶质细胞中连接蛋白43表达的影响。发现向丘脑立体定向注射海藻酸会导致损伤部位连接蛋白43免疫反应性几乎完全缺失。连接蛋白43缺失的区域与那些显示出大量神经元丢失和强烈胶质增生的区域相对应。这些结果表明神经元对星形胶质细胞连接蛋白43表达的调节有贡献，因此，对星形胶质细胞缝隙连接提供的钾空间缓冲能力的局部控制也有贡献。