The balance between stress resilience and vulnerability is regulated by corticotropin-releasing hormone during the critical postnatal period for sensory development

被引:33
作者
Cramer, Tomer [1 ,2 ]
Kisliouk, Tatiana [1 ]
Yeshurun, Shlomo [1 ,2 ]
Meiri, Noam [1 ]
机构
[1] ARO, Dept Poultry & Aquaculture, Inst Anim Sci, Volcani Ctr, IL-50250 Bet Dagan, Israel
[2] Hebrew Univ Jerusalem, Dept Anim Sci, Robert H Smith Fac Agr Food & Environm, IL-76100 Rehovot, Israel
基金
以色列科学基金会;
关键词
stress; thermoregulation; corticotropin-releasing hormone; hypothalamus; chick; EARLY-LIFE STRESS; NEUROTROPHIC FACTOR; DNA METHYLATION; DYNAMIC CHANGES; BRAIN; MECHANISMS; EXPRESSION; ACTIVATION; CRF; GLUCOCORTICOIDS;
D O I
10.1002/dneu.22252
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Determining whether a stressful event will lead to stress-resilience or vulnerability depends probably on an adjustable stress response set point, which is most likely effective during postnatal sensory development and involves the regulation of corticotrophin-releasing hormone (CRH) expression. During the critical period of thermal-control establishment in 3-day-old chicks, heat stress was found to render resilient or sensitized response, depending on the ambient temperature. These two different responses were correlated with the amount of activation of the hypothalamic-pituitary-adrenal (HPA) axis. The expression of CRH mRNA in the hypothalamic paraventricular nucleus was augmented during heat challenge a week after heat conditioning in chicks which were trained to be vulnerable to heat, while it declined in chicks that were trained to be resilient. To study the role of CRH in HPA-axis plasticity, CRH or Crh-antisense were intracranially injected into the third ventricle. CRH caused an elevation of both body temperature and plasma corticosterone level, while Crh-antisense caused an opposite response. Moreover, these effects had long term implications by reversing a week later, heat resilience into vulnerability and vice versa. Chicks that had been injected with CRH followed by exposure to mild heat stress, normally inducing resilience, demonstrated, a week later, an elevation in body temperature, and Crh mRNA level similar to heat vulnerability, while Crh-antisense injected chicks, which were exposed to harsh temperature, responded in heat resilience. These results demonstrate a potential role for CRH in determining the stress resilience/vulnerability balance. (c) 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 842-853, 2015
引用
收藏
页码:842 / 853
页数:12
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