A Sleeping Opportunity Does Not Restore Hippocampal Alterations Induced by 10 Days of Sleep Restriction in Rats

IF 3.8 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Jesús Enrique García-Aviles, Jessica J. Avilez-Avilez, Josué Sánchez-Hernández, Camila Patlán-Márquez, Javier Rodríguez-Alpízar, Fernanda Michell Becerril-Mercado, Adriana Jiménez, Natalí N. Guerrero-Vargas, Jean-Pascal Morin, Melissa Rodríguez-García, Joaquín Manjarrez-Marmolejo, Beatriz Gómez-González, Rosalinda Guevara-Guzmán, Mara A. Guzmán-Ruiz
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引用次数: 0

Abstract

Sleep loss has been implicated in age-related cognitive decline. Experimental sleep restriction (SR) alters the physiology of multiple brain regions and increases blood–brain barrier (BBB) permeability. Among these regions, the hippocampus of both humans and rodents shows alterations that endure longer than in other areas such as the basal ganglia and hypothalamus. In the present study, adult male rats were subjected to 10 days of SR using the modified multiple platform method (MMPM). Immediately after restriction, SR animals exhibited increased IBA-1 immunoreactivity (IR) and cell number, consistent with microglial activation; these morphological changes persisted after a 4 h recovery period. Synaptophysin (Syn) expression was significantly reduced after SR and remained decreased following rest, while the pERK/ERK ratio was significantly increased by the end of the recovery window. These molecular alterations were accompanied by disrupted hippocampal local field potentials (LFPs), characterized by increased alpha and beta activity and reduced delta and theta power. Importantly, SR rats showed impaired short-term memory in the novel object and object location recognition tests after the recovery period. Together, these findings demonstrate that subchronic SR induces persistent microglial and synaptic alterations and abnormal ERK signaling that remain after short rest, correlating with hippocampal network dysfunction and memory impairment.

睡眠机会不能恢复10天睡眠限制引起的大鼠海马改变。
睡眠不足与年龄相关的认知能力下降有关。实验性睡眠限制改变了大脑多个区域的生理机能,增加了血脑屏障(BBB)的渗透性。在这些区域中,人类和啮齿类动物的海马体比基底神经节和下丘脑等其他区域的变化持续的时间更长。本研究采用改良多平台法(MMPM)对成年雄性大鼠进行10天的SR。限制性饮食后,SR动物立即表现出IBA-1免疫反应性(IR)和细胞数量增加,与小胶质细胞活化一致;这些形态变化在恢复期4 h后仍然存在。Synaptophysin (Syn)表达在SR后显著降低,休息后继续降低,而pERK/ERK比值在恢复窗口结束时显著升高。这些分子改变伴随着海马局部场电位(LFPs)的破坏,其特征是α和β活性增加,δ和θ功率降低。重要的是,恢复期后,SR大鼠在新物体和物体位置识别测试中表现出短期记忆受损。总之,这些发现表明,亚慢性SR诱导持续的小胶质细胞和突触改变以及ERK信号异常,这些变化在短暂休息后仍然存在,与海马网络功能障碍和记忆障碍有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neurochemical Research
Neurochemical Research 医学-神经科学
CiteScore
7.70
自引率
2.30%
发文量
320
审稿时长
6 months
期刊介绍: Neurochemical Research is devoted to the rapid publication of studies that use neurochemical methodology in research on nervous system structure and function. The journal publishes original reports of experimental and clinical research results, perceptive reviews of significant problem areas in the neurosciences, brief comments of a methodological or interpretive nature, and research summaries conducted by leading scientists whose works are not readily available in English.
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