Abstract
The present study investigated the role of neuronal nitric oxide synthase (nNOS)/nitric oxide (NO) system in the pathophysiologic regulation of hypoxic–ischemic brain damage (HIBD) in baby rats subjected to electrical stimulation (ES). The motor function, NO concentration in cortex, and protein expressions of nNOS were examined after 14 sessions of ES. Results showed that NO levels in cortex significantly increased 24h after hypoxia–ischemia than sham. ES could improve motor functions in HIBD rats and spontaneously decrease nNOS/NO system. In conclusion, the nNOS/NO pathway might play a critical role as mediator of neuronal recovery in HIBD rats after undergoing ES treatment.
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