Cocaine stimulates adrenocorticotropin (ACTH) secretion through a corticotropin-releasing factor (CRF)-mediated mechanism.
Cocaine was injected intravenously to non-anesthetized, freely moving adult male rats and caused dose-dependent elevations in plasma adrenocorticotropin (ACTH) levels. The observation that this stimulatory effect was completely abolished by pretreatment with a corticotropin-releasing factor (CRF) antiserum, coupled with the lack of effect of cocaine on ACTH secretion by cultured pituitary cells, suggests that cocaine acts within the brain to release endogenous CRF.
Rivier
C
C
Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, CA 92037.
Vale
W
W
D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D003042:Cocaine / Q000494:pharmacology*; D003346:Corticotropin-Releasing Hormone / Q000276:immunology / Q000502:physiology*; D007106:Immune Sera; D007700:Kinetics; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D007106:Immune Sera; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003042:Cocaine