Effect of stressor intensity on habituation and sensitization of glucocorticoid responses in rats.

Abstract

This experiment was designed to study the effect of stressor intensity on habituation/sensitization of the adrenocortical stress response in rats. Rats were given 18 shocks in 3-hr daily sessions for 8 days, and a single shock probe before the sessions was used to determine how adrenocortical responsiveness changed with repeated exposure to the stress sessions. When lower intensity shock was given, the changes in plasma corticosterone response to shock probes followed a U-shaped curve--with a response that first habituated to no-shock control levels but later returned to the same magnitude as seen on the 1st probe day. Plasma corticosterone responses in rats given higher intensity shock never habituated and instead demonstrated an increased response indicative of sensitization; a temporal delay of 1 week occurred before sensitization developed. Responsiveness to exogenous adrenocorticotropin 24 hr after the last stress session was monotonically related to the intensity of the stressor presented during the experimental sessions. These data are consistent with the rule from the habituation literature that stimulus intensity is inversely related to the magnitude of habituation. Thus the data extend the dual process theory of Groves and Thompson (1970) to an endocrine respondent. The data also suggest that an explanation as to discrepancies in the literature concerning adrenocortical response to repeated presentation of stressors may relate to differences in the stressor parameters used.

Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

“…Literature data have shown that frequent stimulation with a low-intensity stressor often leads to habituation of the hypothalamic-pituitary-adrenal axis, while lower frequency and/or high-intensity stimuli can promote an exaggerated response (16). A recent review (17) summarizes the role of the hippocampus in the control of a variety of vegetative functions, such as ACTH secretion, and provides evidence that repeated restraint stress can promote hippocampal atrophy.…”

Effect of vasopressin 1b receptor blockade on the hypothalamic–pituitary–adrenal response of chronically stressed rats to a heterotypic stressor

“…It is known that one aspect of HPA axis plasticity is its ability to show modification in response to the history of previous stressful experiences so that exposure to repeated stress leads to changes in the HPA axis response to subsequent challenges. The characteristics of the stressor, such as intensity ( Natelson et al 1988, Pitman et al 1990, frequency (De Souza & Van Loon 1982, De Boer et al 1990, Ma & Lightman 1998, and nature (i.e. psychological versus physical; for review see (Aguilera et al 1994)) are important in the development of both habituation and sensitization of the HPA axis response to a further challenge with a stressor (see (Dallman 2007) for review).…”

Exposure to Repeated, Intermittent d-amphetamine Induces Sensitization of HPA Axis to a Subsequent Stressor

“…Such manipulations may lead to an increased reactivity to stressors ("sensitization"), which can be expressed both behaviourally and neurochemically (Pitman et al 1990;Badiani et al 1996;Pani et al 2000). One form of sensitization involves the capacity of psychostimulant drugs, such as cocaine and d -amphetamine, to react interchangeably with stressors in producing an augmented behavioral response (Antelman et al 1980;Prasad et al 1998).…”