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

Abstract

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.

Methyl CpG level at distal part of heat‐shock protein promoter HSP70 exhibits epigenetic memory for heat stress by modulating recruitment of POU2F1‐associated nucleosome‐remodeling deacetylase (NuRD) complex

“…These temperatures have been shown to induce, respectively, heat resilience or vulnerability later in life (Cramer et al . ). As depicted in Fig.…”

“…; Cramer et al . ). Sample number (N) includes the number of individual chicks in each treatment group or the number of independent experiments (indicated in ‘Figure Legends’).…”

“…Whereas conditioning of 3‐day‐old chicks under high ambient temperature led to heat vulnerability, mild heat stress induced heat resistance: during heat challenge on day 10 post‐hatch, the body temperature and plasma corticosterone levels of chicks conditioned on day 3 under moderate heat were significantly lower than those of chicks conditioned under high ambient temperature, as well as of those in non‐conditioned chicks (Cramer et al . ). Because ambient heat is expected to increase in the coming decades as a consequence of climate change (Ahuja et al .…”

“…Early-life stress can change neural architecture to increase adverse reactions to stressors, leading to stress -resilience or vulnerability (Franklin et al 2012;Silberman et al 2016). Exposure to heat stress during the critical period of thermalcontrol establishment (between days 3 and 5 post-hatch) in chicks causes long-lasting alterations that contribute to a differential response to subsequent related stimuli (Kisliouk et al 2014;Cramer et al 2015). Whereas conditioning of 3day-old chicks under high ambient temperature led to heat vulnerability, mild heat stress induced heat resistance: during heat challenge on day 10 post-hatch, the body temperature and plasma corticosterone levels of chicks conditioned on day 3 under moderate heat were significantly lower than those of chicks conditioned under high ambient temperature, as well as of those in non-conditioned chicks (Cramer et al 2015).…”

“…Exposure to heat stress during the critical period of thermalcontrol establishment (between days 3 and 5 post-hatch) in chicks causes long-lasting alterations that contribute to a differential response to subsequent related stimuli (Kisliouk et al 2014;Cramer et al 2015). Whereas conditioning of 3day-old chicks under high ambient temperature led to heat vulnerability, mild heat stress induced heat resistance: during heat challenge on day 10 post-hatch, the body temperature and plasma corticosterone levels of chicks conditioned on day 3 under moderate heat were significantly lower than those of chicks conditioned under high ambient temperature, as well as of those in non-conditioned chicks (Cramer et al 2015). Because ambient heat is expected to increase in the coming decades as a consequence of climate change (Ahuja et al 2010;Paital et al 2016), organisms' ability to adapt to thermal challenges will be key to their survival.…”