Exposure to intense noise can trigger a cascade of neuroendocrine events reminiscent of a stress response, including activation of the hypothalamic-pituitary-adrenocortical(HPA) axis. Using male Fischer and Lewis rats, which exhibit differences in their corticosterone response to stressors, this investigation assessed effects of acute noise exposure on neurochemicaland neuroendocrine responses. In response to the noise exposure, Fischer rats displayed greater plasma adrenocorticotropin-releasing hormone (ACTH) and corticosterone responses than their Lewis counterparts. However, both strains responded with similar increases of plasma prolactin, suggesting that strain differences in the HPA response were not likely because of differences in noise perception. Post-mortem analyses revealed that noise exposure induced strain-dependent variations of corticotropin-releasing hormone (CRH) across severalbrain regions. These effects were evident irrespective of whether the rats were noise exposed in a familiar (home cage) or unfamiliar environment. In vivo, dynamic assessment of immunoreactive (ir)-CRH at the pituitary gland revealed that noise exposure elicited an immediate rise in ir-CRH among Fischer rats, relative to the delayed response in Lewis rats. Similarly, the rise in local interstitial corticosterone was more rapid and pronounced in Fischer rats. In contrast to these differences, ir-CRH released at the centralnucleus of the amygdala (CeA) was gradualand protracted following noise exposure in both strains. Behaviorally, the Fischer rats displayed an active stress response, whereas the Lewis strain adopted freezing as a defensive style. The role of CRH in the genesis of the overallstrain-dependent response to stressors is discussed.
- Corticotropin-releasing hormone
- Noise stressor