体育锻炼可介导大脑皮层突触蛋白乳化,从而提高抗压能力。

Cell metabolism Pub Date : 2024-09-03 Epub Date: 2024-08-19 DOI:10.1016/j.cmet.2024.07.018
Lan Yan, Yajie Wang, Haidong Hu, Diran Yang, Wenjing Wang, Zhihua Luo, Yangze Wang, Fengzhen Yang, Kwok-Fai So, Li Zhang
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引用次数: 0

摘要

乳酸盐是人体适应运动训练过程中的一种重要代谢物,它能有效缓解焦虑症。然而,乳酸在运动介导的抗焦虑效应中的生物学机制尚未得到全面研究。在这里,我们报告了运动诱导的乳酸能显著增强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都表明,SNAP91的乳酰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,赋予了对慢性束缚应激(CRS)的恢复力。更有趣的是,运动促进的 SNAP91 乳酰化是预防 CRS 小鼠焦虑样行为的必要条件。这些结果共同表明,大脑中的非组蛋白乳酰化是以前未曾认识到的调节精神功能的方法,并为大脑在运动范例中的代谢适应提供了证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Physical exercise mediates cortical synaptic protein lactylation to improve stress resilience.

Physical exercise mediates cortical synaptic protein lactylation to improve stress resilience.

Lactate is a critical metabolite during the body's adaption to exercise training, which effectively relieves anxiety-like disorders. The biological mechanism of lactate in the exercise-mediated anxiolytic effect has, however, not been comprehensively investigated. Here, we report that exercise-induced lactate markedly potentiates the lactylation of multiple synaptic proteins, among which synaptosome-associated protein 91 (SNAP91) is the critical molecule for synaptic functions. Both anatomical evidence and in vivo recording data showed that the lactylation of SNAP91 confers resilience against chronic restraint stress (CRS) via potentiating synaptic structural formation and neuronal activity in the medial prefrontal cortex (mPFC). More interestingly, exercise-potentiated lactylation of SNAP91 is necessary for the prevention of anxiety-like behaviors in CRS mice. These results collectively suggest a previously unrecognized non-histone lactylation in the brain for modulating mental functions and provide evidence for the brain's metabolic adaption during exercise paradigms.

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