The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone

Abstract

Both intracerebroventricular (i.c.v.) IL-1β and exposure to inescapable tail shock (IS) activate acute phase responses (APRs) that include increases in core body temperature (CBT), increases in hypothalamic–pituitary–adrenal activity, decreases in carrier proteins such as corticosterone binding globulin (CBG), aphagia and adipsia. A variety of data suggested that stressors produce APRs by inducing brain IL-1β. The current series of studies further explored this possibility by determining whether the functional IL-1β antagonist, α-melanocyte-stimulating hormone (α-MSH (1–13)), would block IS-induced APRs. Immediately following i.c.v. α-MSH (1–13) administration, rats were exposed to a single session of 100, 5 s, 1.6 mA ISs, or control treatment (home cage control). α-MSH (1–13) blocked IS-induced increased CBT, increased plasma corticosterone (CORT), decreased CBG, aphagia and adipsia 24 h after IS. The inhibitory effects of α-MSH (1–13) were shown not to be a consequence of α-MSH (1–13) producing its actions 24 h after its administration because α-MSH (1–13) given 24 h before IS did not block IS-induced increased CBT and CORT during IS. Additionally, α-MSH (1–13), given 24 h before IS, had no effect on increased CBT, increased CORT, decreased CBG, adipsia, or aphagia 24 h after IS. These data provide support for a specific mode of action for i.c.v. α-MSH (1–13), namely blockade of APRs with no impact on acute hyperthermia or increased levels of CORT produced during IS.