Stressful events affect numerous physiological processes including central nervous system and endocrine responses. Repeated stress alters basic mechanisms for the maintenance of hypothalamic-pituitary-adrenocortical (HPA) homeostasis. The purpose of the present study was to determine whether, and to what extent prior repeated restraint or social crowding stress during 3 days affects the HPA response to an acute short-lasting restraint stress. Male Wistar rats were restrained 2 times a day for 3 days or subjected to crowding stress for 3 days before exposure to acute restraint stress in metal tubes for 10 min. Immediately after the restraint or 1 h, 2 and 3 h later the rats were decapitated and their trunk blood was collected for the measurement of plasma ACTH and corticosterone levels. Chronic stress alone (restraint 2 x 10 min/day for 3 days and crowding for 3 days) induced a moderate increase in plasma ACTH level compared to the corresponding level in control rats without prior stress exposure. Acute restraint stress for 10 min considerably increased plasma corticosterone and ACTH levels immediately after restraint and no substantial increase was observed 1, 2 or 3 h after stressor termination. Restraint and crowding for 3 days significantly and to a similar extent inhibited the restraint stress-induced increase in ACTH and corticosterone secretion. These results indicate that repeated restraint or crowding stress potently attenuates the acute restraint stress-induced stimulatory action of the HPA axis what suggests adaptive action of moderate stress on the HPA axis response to acute stress. The results also suggest that a short-lasting hypersecretion of corticosterone during psychological stress may induce a prolonged feedback inhibition of the HPA axis activity.
Grant: POIG 01.01.02-12-004/09-00 financed by European Regional Development Fund.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported however funding details unavailable.
05 - 09 May 2012
European Society of Endocrinology