Chronic social isolation in adaptation of HPA axis to heterotypic stress.

Abstract

Social crowding and isolation are recognized as major stressors and risk factors for development of psychiatric disorders. Chronic isolation stress (IS) and crowding stress (CS) activate neuroendocrine and neurochemical mechanisms, that activate the hypothalamic-pituitary-adrenal (HPA) axis. Changes of the plasma level of interleukin-1β (IL-1β), ACTH and corticosterone (CORT) after chronic psychosocial IS and CS were investigated. Control rats were kept 5 per cage and not stressed. Stressed groups were subjected to either CS for 3, 7, 14days+restraint stress (RS) or IS for (11days) before this treatment was applied. Crowded rats were remained (24 in one cage) and RS rats were restrained for 10min. Total CORT, ACTH and IL-1β levels were measured using commercially available kits. Social CS for 3days significantly increased plasma IL-1β level. Social IS increased plasma IL-1β level after longer period of subsequent CS 7 and 14days, than ACTH and CORT, after 3 and 7days. Prior IS significantly increased plasma IL-1β level induced by subsequent combined CS for 3days+acute RS, but significantly or totally inhibited the acute stress-induced increase of plasma IL-1β level after 7 and 14days of combined stress. IS, by contrast, strongly inhibited the increase of plasma ACTH and CORT level induced by combined CS+acute RS. Chronic IS augments the changes of IL-1β level induced by a longer crowding period than ACTH and CORT. Modulatory action of IL-1β and pituitary-adrenocortical hormones adaptation to chronic social stress is asynchronous.