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体育锻炼通过促进皮层突触蛋白的乳酸化改善压力耐受性
作者:小柯机器人 发布时间:2024/8/24 23:25:54

暨南大学张力课题组发现,体育锻炼通过促进皮层突触蛋白的乳酸化改善压力耐受性。相关论文于2024年8月19日在线发表于国际学术期刊《细胞—代谢》。

研究人员报告了运动诱导的乳酸显著增强了多种突触蛋白的乳酸化作用,其中突触体相关蛋白91(SNAP91)是突触功能的关键分子。解剖学证据和体内记录数据均显示,SNAP91的乳酸化通过增强内侧前额叶皮层(mPFC)的突触结构形成和神经元活动,赋予对慢性束缚应激(CRS)的耐受性。

更有趣的是,运动增强的SNAP91乳酸化对于预防CRS小鼠的类焦虑行为是必要的。这些结果共同表明了一种此前未被认识的脑中非组蛋白乳酸化在调节精神功能中的作用,并提供了大脑在运动过程中代谢适应的证据。

据介绍,乳酸是身体适应运动训练过程中关键的代谢物,有效缓解类焦虑障碍。然而,乳酸在运动介导的抗焦虑效应中的生物机制尚未得到全面研究。

附:英文原文

Title: Physical exercise mediates cortical synaptic protein lactylation to improve stress resilience

Author: Lan Yan, Yajie Wang, Haidong Hu, Diran Yang, Wenjing Wang, Zhihua Luo, Yangze Wang, Fengzhen Yang, Kwok-Fai So, Li Zhang

Issue&Volume: 2024-08-19

Abstract: Lactate is a critical metabolite during the body’s adaption to exercise training,which effectively relieves anxiety-like disorders. The biological mechanism of lactatein the exercise-mediated anxiolytic effect has, however, not been comprehensivelyinvestigated. Here, we report that exercise-induced lactate markedly potentiates thelactylation of multiple synaptic proteins, among which synaptosome-associated protein91 (SNAP91) is the critical molecule for synaptic functions. Both anatomical evidenceand in vivo recording data showed that the lactylation of SNAP91 confers resilience against chronicrestraint stress (CRS) via potentiating synaptic structural formation and neuronalactivity in the medial prefrontal cortex (mPFC). More interestingly, exercise-potentiatedlactylation of SNAP91 is necessary for the prevention of anxiety-like behaviors inCRS mice. These results collectively suggest a previously unrecognized non-histonelactylation in the brain for modulating mental functions and provide evidence forthe brain’s metabolic adaption during exercise paradigms.

DOI: 10.1016/j.cmet.2024.07.018

Source: https://www.cell.com/cell-metabolism/abstract/S1550-4131(24)00289-4

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:31.373
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx