Effects of Prepubertal Stress on Subsequent Acth Response to Novel Stress and CRH in Male vs Female Rats

Abstract

The effects of long‐term chronic stress during prepubertal periods of growth and development on an organism's ability to release ACTH during future episodes of an acute novel stress and in response to exogenous CRH were examined. Following a 6‐week stress period, in which prepubertal male and female WKY rats were subjected to three different and randomly given stress paradigms (heat, noise and immobilization) at various times of the day (in order to prevent adaptation to stress), chronically stressed male rats were far less able to respond to CRH plus a novel ether stress than were their male controls or their female counterparts. Although baseline ACTH levels were similar in both male and female control and experimental rats, when subjected to a subsequent acute ether stress, the differences in ACTH response between controls and experimentals as well as between males and females were significant. ACTH response to stressors was significantly blunted in both male and female experimental rats compared to their controls, but the male response was significantly lower than that of the females. These results suggest that prepubertal chronic stress may permanently alter an organism's ability to release ACTH, even when subjected to a novel and traumatic ether stress, and that males may be much more susceptible than females to prepubertal stress. Long‐term stress, therefore, if experienced during critical developmental periods such as preadolescence, can permanently damage the stress response mechanism and cause other, more serious physiological disorders.

Temperament moderates the influence of periadolescent social experience on behavior and adrenocortical activity in adult male rats

“…This alteration in adult glucocorticoid production was documented more than 2-months following the adolescent social experience suggesting that there was a long-term recalibration of adrenocortical activity. Similar findings of adult hypothalamic-pituitary-adrenal (HPA) hyporeactivity have been documented in humans and rodents that experienced more severe physical and social stressors during adolescence or adulthood (e.g., four to six weeks of exposure to immobilization, change of cage mate, cage tilt, exposure to white noise, exposure to predator odor; Bazak et al, 2009; Goliszek et al, 1996; Toth et al, 2008; Schmidt et al, 2007; Engert et al, 2010; Rós-Simo & Valverde, 2012; Ostrander et al, 2006). Fries, Hesse, Hellhammer, and Hellhammer (2005) proposed that chronic stress exposure may lead to an initial period of glucocorticoid hypersecretion followed by subsequent HPA hypoactivity.…”

Adolescent activity-based anorexia increases anxiety-like behavior in adulthood

“…For example, male rats exposed to repeated stressors during adolescence displayed blunted hormonal responses to novel stressors in adulthood [38]. While most studies of adolescent stress exposure have been conducted in male rats, there is increasing evidence of gender-specific effects.…”

Pituitary dysmaturation affects psychopathology and neurodevelopment in 22q11.2 Deletion Syndrome

“…Our results are the first to suggest atypical HPAA maturation in single longitudinal sample of individuals with 22q11DS. The observation that PitVol reductions emerge during late adolescence might be related to the ongoing maturation of the negative feedback exerted by cortisol on the ACTH secretion, reported during adolescence in animal models (Andrew G. Goliszek, 1996).…”

“…This mechanism is thought to account for increased PitVol observed in early stages of psychosis (Pariante, 2008). However, chronic stress in animals can lead to reduced pituitary ACTH secretion and hypocortisolism in response to a novel stressor (Andrew G. Goliszek, 1996;Houshyar et al, 2001). Such hypocortisolism has been attributed to an enhanced negative feedback on pituitary ACTH secretion exerted by chronic elevated cortisol (Houshyar et al, 2001).…”