Cramer Tomer, Kisliouk Tatiana, Yeshurun Shlomo, Meiri Noam
Department of Poultry and Aquaculture, Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, 50250, Israel.
The Robert H. Smith Faculty of Agriculture, Food and Environment, Department of Animal Science, the Hebrew University of Jerusalem, Rehovot, 76100, Israel.
Dev Neurobiol. 2015 Aug;75(8):842-53. doi: 10.1002/dneu.22252. Epub 2014 Dec 10.
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.
确定一个应激事件是否会导致应激恢复力或易感性可能取决于一个可调节的应激反应设定点,该设定点在出生后的感觉发育期间最有可能起作用,并且涉及促肾上腺皮质激素释放激素(CRH)表达的调节。在3日龄雏鸡建立体温调节的关键时期,发现热应激会产生恢复性或敏感性反应,这取决于环境温度。这两种不同的反应与下丘脑-垂体-肾上腺(HPA)轴的激活程度相关。在经过热训练而变得易受热应激影响的雏鸡中,热适应一周后在热刺激期间,下丘脑室旁核中CRH mRNA的表达增加,而在经过训练具有恢复力的雏鸡中其表达则下降。为了研究CRH在HPA轴可塑性中的作用,将CRH或Crh反义寡核苷酸颅内注射到第三脑室。CRH导致体温和血浆皮质酮水平升高,而Crh反义寡核苷酸则产生相反的反应。此外,这些作用具有长期影响,一周后会发生逆转,将热恢复力转变为易感性,反之亦然。注射CRH后再暴露于轻度热应激(通常会诱导恢复力)的雏鸡,一周后表现出体温升高,并且Crh mRNA水平类似于热易感性,而注射Crh反义寡核苷酸的雏鸡在暴露于严酷温度时则表现出热恢复力。这些结果证明了CRH在确定应激恢复力/易感性平衡中具有潜在作用。