Differential pattern of expression of voltage-gated sodium channel genes following ischemic brain injury in rats.
This study investigated the effects of brain ischemia on sodium channel gene (NaCh) expression in rats. Using quantitative RT-PCR, our findings demonstrated the expression ratio of NaCh genes in normal rat brain to be Na(v)1.1 > Na(v)1.8 > Na(v)1.3 > Na(v)1.7 (rBI > PN3 > rBIII > PN1). In contrast, brain injury caused by middle cerebral artery occlusion (MCAo) for 2 h followed by reperfusion significantly down-regulated Na(v)1.3 and Na(v)1.7 genes in both injured and contralateral hemispheres; whereas the Na(v)1.8 gene was down regulated in only the injured hemisphere (though only acutely at 2 or 2-6 h post-MCAo). However, the time-course of NaCh gene expression revealed a significant down-regulation of Na(v)1.1 only in the ischemic hemisphere beginning 6 h post-MCAo and measured out to 48 h post-MCAo. In a separate preliminary study Na(v)1.2 (rBII) gene was found to be expressed at levels greater than that of Na(v)1.1 in normal rats and was significantly down regulated at 24 h post-MCAo). Our findings document, for the first time, quantitative and relative changes in the expression of various NaCh genes following ischemic brain injury and suggest that the Na(v)1.1 sodium channel gene may play a key role in ischemic injury/recovery.
Yao
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Division of Neurosciences, Walter Reed Army Institute of Research, Silver Spring, MD 20910-7500, USA. Jit.dave@na.amedd.army.mil
Williams
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Cui
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Berti
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Hunter
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Tortella
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Dave
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