Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5736397 | Brain Research Bulletin | 2017 | 8 Pages |
Abstract
Focal ischemic stroke can lead to brain damage and cause human disability and death. Increased excitatory transmission and reduced neuronal inhibition are important pathological alterations in the cerebral ischemia, which can induce abnormal brain excitability. Nav1.6 is a key determinant of neuronal excitability in the nervous system. Here we investigate the expression of Nav1.6 at protein and mRNA levels in the rats subjected to middle cerebral artery occlusion (MCAO). Nav1.6 expression at mRNA levels in the ischemic and contralateral hemispheres of MCAO rats were persistently decreased at 6Â h, 12Â h and 24Â h after reperfusion compared to the sham-operated rats. However, a prominent, dynamic increase of Nav1.6 immunoreactivity in reactive astrocytes was observed in the genu of corpus callosum (GCC) of MCAO rats in the acute phase, reaching the peak at 6Â h after reperfusion, rapidly dropping at 12Â h and 24Â h after reperfusion. Furthermore, the upregulation of Nav1.6 expression was strongly correlated with the severity of reactive astrogliosis. Collectively, these findings suggest that this upregulated astrocytic sodium channel expression in the GCC of MCAO rats may contribute to the functional roles of reactive astrocytes in response to brain ischemia.
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Authors
Hongyan Zhu, Weide Lin, Yuxiao Zhao, Ziyi Wang, Wenwen Lao, Ping Kuang, Houguang Zhou,