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 6 h, 12 h and 24 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 6 h after reperfusion, rapidly dropping at 12 h and 24 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.
[1]Shanghai Univ, Sch Life Sci, Nanchen Rd 333, Shanghai 200444, Peoples R China.
[2]Fudan Univ, Huashan Hosp, Dept Geriatr Neurol, Middle Wulumuqi Rd, Shanghai 200040, Peoples R China.
(8.0+极速模式)