帕尔瓦布明
创伤性脑损伤
乙酰半胱氨酸
氧化应激
神经周围网
中间神经元
神经保护
医学
神经科学
麻醉
心理学
内科学
抑制性突触后电位
生物
精神科
抗氧化剂
生物化学
作者
Mustafa Q. Hameed,Nathaniel Hodgson,Henry H.C. Lee,A. Pascual-Leone,Paul MacMullin,Ali Jannati,Sameer C. Dhamne,Takao K. Hensch,Alexander Rotenberg
出处
期刊:Cerebral Cortex
[Oxford University Press]
日期:2022-09-20
卷期号:33 (7): 4070-4084
被引量:3
标识
DOI:10.1093/cercor/bhac327
摘要
Abstract Traumatic brain injury (TBI) increases cerebral reactive oxygen species production, which leads to continuing secondary neuronal injury after the initial insult. Cortical parvalbumin-positive interneurons (PVIs; neurons responsible for maintaining cortical inhibitory tone) are particularly vulnerable to oxidative stress and are thus disproportionately affected by TBI. Systemic N-acetylcysteine (NAC) treatment may restore cerebral glutathione equilibrium, thus preventing post-traumatic cortical PVI loss. We therefore tested whether weeks-long post-traumatic NAC treatment mitigates cortical oxidative stress, and whether such treatment preserves PVI counts and related markers of PVI integrity and prevents pathologic electroencephalographic (EEG) changes, 3 and 6 weeks after fluid percussion injury in rats. We find that moderate TBI results in persistent oxidative stress for at least 6 weeks after injury and leads to the loss of PVIs and the perineuronal net (PNN) that surrounds them as well as of per-cell parvalbumin expression. Prolonged post-TBI NAC treatment normalizes the cortical redox state, mitigates PVI and PNN loss, and - in surviving PVIs - increases per-cell parvalbumin expression. NAC treatment also preserves normal spectral EEG measures after TBI. We cautiously conclude that weeks-long NAC treatment after TBI may be a practical and well-tolerated treatment strategy to preserve cortical inhibitory tone post-TBI.
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