作者: Zhigang Lei , Ping Deng , Jinqing Li , Zao C. Xu
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摘要: Traumatic brain injury (TBI) is associated with cognitive deficits, memory impairment, and epilepsy. Previous studies have reported neuronal loss hyperexcitability in the post-traumatic hippocampus. A-type K+ currents (I(A)) play a critical role modulating intrinsic membrane excitability of hippocampal neurons. The disruption I(A) reportedly linked to dysfunction. present study investigates changes hippocampus after TBI. TBI rats was induced by controlled cortical impact. impact reproducible lesion cortex an obvious death ipsilateral CA3 region. At one week TBI, immunohistochemical staining Western blotting showed that expression channel subunit Kv4.2 markedly decreased hippocampus, but remained unchanged contralateral Meanwhile, electrophysiological recording CA1 pyramidal neurons were significantly reduced, which increased excitability. Furthermore, there sensitivity bicuculline-induced seizures rats. 8 weeks indicated returned control levels. These findings suggest causes transient downregulation neurons, might be turn leads