Oxidative Stress-mediated Loss of Hippocampal Parvalbumin Interneurons Contributes to Memory Precision Decline After Acute Sleep Deprivation.

Autor: Gao YZ; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., Liu K; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., Wu XM; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., Shi CN; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., He QL; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., Wu HP; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China., Yang JJ; Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. yjyangjj@126.com., Yao H; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China. yaohao@njmu.edu.cn., Ji MH; Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China. jimuhuo2009@sina.com.
Jazyk: angličtina
Zdroj: Molecular neurobiology [Mol Neurobiol] 2024 Nov 15. Date of Electronic Publication: 2024 Nov 15.
DOI: 10.1007/s12035-024-04628-0
Abstrakt: Sleep is pivotal to memory consolidation, and sleep deprivation (SD) after learning can impede this process, leading to memory disorders. In the present study, we aimed to explore the effects of acute sleep deprivation (ASD) on memory disorders and the underlying mechanisms. ASD model was induced by subjecting the mice to 6 h of SD following fear conditioning training. Different cohorts were used for behavioral, biochemical, and electrophysiological tests. Here, we showed that memory precision decline was induced by ASD, concomitant with a notable elevation in oxidative stress within PV interneurons, loss of PV, and disturbed neuronal oscillation in the CA1 region. Notably, chemogenetic activation of PV interneurons effectively ameliorated abnormal gamma oscillation and memory precision decline observed in ASD mice. Meanwhile, chemogenetic inhibition of PV interneurons successfully mimicked the abnormal brain oscillations and memory precision decline observed in ASD mice. Additionally, prior administration of the antioxidant medication N-acetylcysteine effectively reversed memory precision decline and mitigated PV loss and abnormal oscillation triggered by ASD. Collectively, our findings indicated that ASD increased oxidative stress in PV interneurons, thereby disrupting neural oscillation in the CA1 and ultimately leading to memory precision decline.
Competing Interests: Declarations Ethics Approval All the animal experiments were approved by the Ethics Committee of Nanjing Medical University, and all procedures were performed in accordance with the approved guidelines. Consent to Participate Not applicable. Consent for Publication Not applicable. Competing Interests The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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