Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both intracerebroventricular (i.c.v.) IL-1beta 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-1beta. The current series of studies further explored this possibility by determining whether the functional IL-1beta antagonist, alpha-melanocyte-stimulating hormone (alpha-MSH(1-13)), would block IS-induced APRs. Immediately following i.c.v. alpha-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). alpha-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 alpha-MSH(1-13) were shown not to be a consequence of alpha-MSH(1-13) producing its actions 24 h after its administration because alpha-MSH(1-13) given 24 h before IS did not block IS-induced increased CBT and CORT during IS. Additionally, alpha-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. alpha-MSH(1-13), namely blockade of APRs with no impact on acute hyperthermia or increased levels of CORT produced during IS.
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PMID:The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone. 981 38