Lucassen Paul J, Oomen Charlotte A, Naninck Eva F G, Fitzsimons Carlos P, van Dam Anne-Marie, Czeh Boldizsár, Korosi Aniko
Centre for Neuroscience, Swammerdam Institute of Life Sciences, University of Amsterdam, 1090 GE Amsterdam, The Netherlands.
VU University Medical Center, Department of Anatomy & Neurosciences, 1007 MB Amsterdam, The Netherlands.
Cold Spring Harb Perspect Biol. 2015 Sep 1;7(9):a021303. doi: 10.1101/cshperspect.a021303.
Exposure to stress is one of the best-known negative regulators of adult neurogenesis (AN). We discuss changes in neurogenesis in relation to exposure to stress, glucocorticoid hormones, and inflammation, with a particular focus on early development and on lasting effects of stress. Although the effects of acute and mild stress on AN are generally brief and can be quickly overcome, chronic exposure or more severe forms of stress can induce longer lasting reductions in neurogenesis that can, however, in part, be overcome by subsequent exposure to exercise, drugs targeting the stress system, and some antidepressants. Exposure to stress, particularly during the sensitive period of early life, may (re)program brain plasticity, in particular, in the hippocampus. This may increase the risk to develop cognitive or anxiety symptoms, common to brain diseases like dementia and depression in which plasticity changes occur, and a normalization of neurogenesis may be required for a successful treatment response and recovery.
暴露于应激是成人神经发生(AN)最广为人知的负调节因子之一。我们讨论了与暴露于应激、糖皮质激素和炎症相关的神经发生变化,特别关注早期发育以及应激的长期影响。虽然急性和轻度应激对AN的影响通常是短暂的,并且可以迅速克服,但长期暴露或更严重形式的应激会导致神经发生的持久减少,然而,随后进行运动、使用针对应激系统的药物和一些抗抑郁药,部分可以克服这种减少。暴露于应激,尤其是在生命早期的敏感期,可能会(重新)编程大脑可塑性,特别是在海马体中。这可能会增加出现认知或焦虑症状的风险,这些症状在痴呆和抑郁症等脑部疾病中很常见,其中会发生可塑性变化,并且成功的治疗反应和恢复可能需要神经发生正常化。