Synaptic rewiring of stress-sensitive neurons by early-life experience: A mechanism for resilience?

Neurobiology of Stress

Jenny Molet¹  Tallie Z. Baram²  Benjamin G. Gunn²  Akanksha Singh-Taylor²  Aniko Korosi³ 

[1] Department of Anatomy/Neurobiology, University of California-Irvine, Irvine, CA 92697-4475, USA;Department of Pediatrics, University of California-Irvine, Irvine, CA 92697-4475, USA;Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, 1098 XH Amsterdam, The Netherlands;

关键词: Synaptic plasticity;    Resilience;    Stress;    Corticotropin releasing hormone (CRH);    Maternal care;    Epigenetics;   

DOI  :  10.1016/j.ynstr.2014.10.007

来源: DOAJ

【 摘 要 】

Genes and environment interact to influence cognitive and emotional functions throughout life. Early-life experiences in particular contribute to vulnerability or resilience to a number of emotional and cognitive illnesses in humans. In rodents, early-life experiences directly lead to resilience or vulnerability to stress later in life, and influence the development of cognitive and emotional deficits. The mechanisms for the enduring effects of early-life experiences on cognitive and emotional outcomes are not completely understood. Here, we present emerging information supporting experience-dependent modulation of the number and efficacy of synaptic inputs onto stress-sensitive neurons. This synaptic ‘rewiring’, in turn, may influence the expression of crucial neuronal genes. The persistent changes in gene expression in resilient versus vulnerable rodent models are likely maintained via epigenetic mechanisms. Thus, early-life experience may generate resilience by altering synaptic input to neurons, which informs them to modulate their epigenetic machinery.

【 授权许可】

Unknown