Developmental loss of parvalbumin-positive cells in the prefrontal cortex and psychiatric anxiety after intermittent hypoxia exposures in neonatal rats might be mediated by NADPH oxidase-2.
作者： Dong Liang , Guowei Li , Xingzhi Liao , Dawei Yu , Jing Wu
DOI: 10.1016/J.BBR.2015.08.033
关键词:
摘要: Sleep apnea is more frequently experienced in neonatal life. Here we investigated the causal contribution of NOX2-derived oxidative stress prefrontal cortex (PFC) to neurodevelopmental alterations and psychiatric anxiety a rat model sleep apnea. Neonatal postnatal day 5 (P5) rats were exposed long-term intermittent hypoxia (LTIH) or room air (RA) for 10 days. In PFC, determined impact (I) LTIH exposures on NADPH oxidase-2 (NOX2) expression (II) pharmacological NOX2 inhibition LTIH-induced P14 P49 rats. Endpoints stress, parvalbumin (PV)-positive cells (PV-cells) anxiety. The results showed increased PFC rats, which was accompanied with elevation NOX activity. cortical PV-cells characterized by 8-hydroxy-20-deoxyguanosine (8-OHDG) level reduced PV immunoreactivity, PV-cell counts levels Pretreatment before each exposure antioxidant/NOX inhibitor apocynin prevented loss development anxiety-like behavior. Our data suggest that might be involved developmental LTIH.
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