Differential Impact of Audiogenic Stressors on Lewis and Fischer Rats: Behavioral, Neurochemical, and Endocrine Variations

Abstract

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 neurochemical and 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 several brain 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 central nucleus of the amygdala (CeA) was gradual and 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 overall straindependent response to stressors is discussed.

Brainstem origins of glutamatergic innervation of the rat hypothalamic paraventricular nucleus

“…The present data suggest a role for glutamate in this projection. Moreover, the present evidence for dual-labeled neurons within the sub-parafascicular nucleus is consistent with a previous study implicating the region in responsiveness to audiogenic stress (Campeau and Watson, 2000), a stressor known to activate both PVH neurons and the HPA axis (Burow et al, 2005; Campeau and Watson, 1997, 2000; Helfferich and Palkovits, 2003; Michaud et al, 2003; Palkovits et al, 2004). Thus, the present findings support the possibility that audiogenic stress activates the PVH and HPA axis via glutamatergic PVH projections.…”

Behavior and pro-inflammatory cytokine variations among submissive and dominant mice engaged in aggressive encounters: moderation by corticosterone reactivity.

“…Consistent with these reports, as well as earlier studies (Bartolomucci et al, 2001; Becker et al, 2008; Audet and Anisman, 2009), aggressive encounters markedly increased plasma corticosterone levels, and this effect was still evident in some mice 75 min after the confrontation, a time at which corticosterone elevations induced by most stressors have normalized (Sapolsky et al, 2000; Michaud et al, 2003). In other mice, however, corticosterone levels 75 min after aggressive episodes were comparable to that of non-stressed animals.…”

Effect of noise pollution on testicular tissue and hormonal assessment in rat

“…Noise stress has an effect on the activity of neuropeptides in hypothalamic and extrahypothalamic sites and significantly it causes an increase in the secretion of hypothalamic hormones such as CRH and ACTH (Michaud et al ., ). In addition to extra hypothalamic effects, these hormones increase the activity of the HTPA axis and stimulate release of corticosterone such as cortisol from the adrenal cortex (Spreng, ).…”