Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress.
The purpose of the present study was to assess whether, and to what extent prior handling, restraint or social crowding stress during 3-10 days affects the hypothalamic-pituitary-adrenocortical (HPA) response to an acute short-lasting restraint stress. Also the effect of a feedback inhibitory mechanism of corticosterone in the impairment of HPA axis by these stressors was investigated. Male Wistar rats were pretreated with handling 1 min/day for 3-10 days, restraint 2 times daily for 3-7 days and crowding stress for 7 days before exposure to acute restraint stress in metal tubes for 10 min. Some group of rats received exogenous s.c. corticosterone either once 25 mg/kg or 2 times daily 10 mg/kg for 3-10 days before restraint stress. After the last restraint the rats were decapitated and their trunk blood was collected for the measurement of plasma ACTH and serum corticosterone levels. Handling for 3-7 days, restraint for 3-7 days, and crowding for 7 days and a single pretreatment with corticosterone--all significantly and to a similar extent inhibited the restraint stress-induced increase in ACTH and corticosterone secretion. Chronic pretreatment with corticosterone blunted the restraint stress-induced increase in HPA axis activity. These results indicate that repeated short-lasting stress induced by handling, restraint, or crowding potently attenuates the acute restraint stress-induced stimulatory action of the HPA axis. They also indicate 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. The attenuation of HPA axis response by prior handling has also obvious methodological implications.
Gadek-Michalska
A
A
Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Bugajski
J
J
D000222:Adaptation, Physiological / Q000187:drug effects / Q000502:physiology; D000324:Adrenocorticotropic Hormone / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism; D000818:Animals; D003345:Corticosterone / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000097:blood / Q000494:pharmacology; D003441:Crowding / Q000503:physiopathology*; D004334:Drug Administration Schedule; D025461:Feedback, Physiological / Q000187:drug effects / Q000502:physiology; D006234:Handling, Psychological; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000503:physiopathology*; D007279:Injections, Subcutaneous; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000379:methods*; D013312:Stress, Physiological / Q000503:physiopathology* / Q000517:prevention & control; D013997:Time Factors
D000324:Adrenocorticotropic Hormone; C029939:corticosterone acetate; D003345:Corticosterone