德国马克斯·普朗克精神病学研究所的研究发现，压力激素皮质促肾上腺激素释放激素（CRH）在脑损伤修复中发挥关键作用[1]。研究人员发现，约三分之一的少突胶质细胞前体细胞（OPCs）在脑损伤部位激活CRH，这种激素反应在损伤后数小时内可被检测到，但约三天后会关闭[1]。这一机制有助于控制这些细胞的成熟并重建保护性神经髓鞘[1]。
缺少CRH受体1会改变这一过程的效果[1]。实验表明，缺少CRH受体1时，少突胶质细胞前体增殖更快但最终产生的成熟少突胶质细胞更少[1]。进一步的研究发现，缺少CRH受体1的小鼠在脑发育早期产生更多少突胶质细胞前体，成年后髓鞘厚度增加，特别是在细轴突周围[1]。
研究团队负责人Clemens Ries和Jan Deussing推测，CRH系统在抑郁症等压力相关精神障碍中可能发挥比已知更重要的作用[1]。这一发现为理解早期压力如何导致精神障碍提供了新的线索[1]。相关研究成果已发表在《Cell Reports》期刊2025年第44卷第11期[1]。
Researchers at Germany's Max Planck Institute of Psychiatry have identified a mechanism by which a stress hormone facilitates brain self-repair after injury.[1] The study found that oligodendrocyte progenitor cells (OPCs) rapidly release corticotropin-releasing hormone (CRH) at sites of brain damage, where it helps regulate the maturation of these cells and the reconstruction of protective myelin sheaths around nerve fibers.[1] Approximately one-third of OPCs activate CRH in response to brain injury, with the hormone response detectable within hours but typically shutting down after about three days.[1]
To understand CRH's role, researchers examined mice lacking CRH receptor 1.[1] These animals showed faster OPC proliferation immediately following injury, yet ultimately produced fewer mature oligodendrocytes than normal mice.[1] The findings also revealed broader implications for early brain development: mice without CRH receptor 1 generated more OPCs during early development and exhibited thicker myelin in adulthood, particularly around smaller nerve fibers.[1] According to researchers Clemens Ries and Jan Deussing, the CRH system may play a more significant role in stress-related psychiatric disorders such as depression than previously understood.[1] The research was published in Cell Reports, volume 44, issue 11, in 2025.[1]