Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus

被引:36
|
作者
Manley, Nathan C. [1 ]
Bertrand, Anthony A. [1 ]
Kinney, Kevin S. [4 ]
Hing, Tressia C. [1 ]
Sapolsky, Robert M. [1 ,2 ,3 ]
机构
[1] Stanford Univ, Gilbert Lab, Dept Biol Sci, Stanford, CA 94305 USA
[2] Stanford Univ, Med Ctr, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[3] Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA
[4] Depauw Univ, Dept Biol, Greencastle, IN 46135 USA
关键词
monocyte chemoattractant protein-1; blood-brain barrier; leukocyte recruitment; kainic acid; hippocampus; epilepsy;
D O I
10.1016/j.brainres.2007.08.092
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Brain injury due to seizure induces a robust inflammatory response that involves multiple factors. Although the expression of chemokines has been identified as a part of this response, there are remaining questions about their relative contribution to seizure pathogenesis. To address this, we report the expression profile of the chemokine, monocyte chemoattractant protein-1 (MCP-1, CCL2), during kainate-induced seizure in the rat hippocampus. Furthermore, we compare MCP-1 expression to the temporal profile of blood-brain barrier (BBB) permeability and immune cell recruitment at the injury site, since both of these events have been linked to MCP-1. We find that BBB permeability increased prior to upregulation of MCP-1, while MCP-1 upregulation and immune cell recruitment occurred concurrently, 7-13 h after opening of the BBB. Our findings support the following conclusions: (1) BBB opening to large proteins does not require MCP-1 upregulation; (2) Leukocyte immigration is not sufficient to induce BBB opening to large proteins; (3) MCP-1 upregulation likely mediates recruitment of macrophages/microglia and granulocytes during seizure injury, thus warranting further investigation of this chemokine. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:138 / 143
页数:6
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