ACTH1-24 effects on d-amphetamine self-administration and the dynamics of brain dopamine in rats.
The present experiments investigated the role of ACTH fragments in d-amphetamine self-administration in rats. Presession injections of 20 or 40 ug/80 ul ACTH1-24 (but not 10 ug/80 ul ACTH1-24 nor any dose of ACTH4-10) significantly reduced rates of d-amphetamine self-infusion for 2 days. Neurochemical experiments revealed that ACTH1-24, followed 24hr later by haloperidol, attenuated haloperidol-induced increases in HVA and DOPAC in both the caudate and nucleus accumbens. It was tentatively concluded that the corticosteroid mediated neuromodulatory action of ACTH1-24 on dopaminergic neurons might increase the rewarding quality of d-amphetamine, thus rendering control levels of self-infusion superfluous.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000031:analogs & derivatives*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D002421:Caudate Nucleus / Q000378:metabolism; D003216:Conditioning, Operant / Q000187:drug effects*; D003366:Cosyntropin / Q000494:pharmacology*; D003913:Dextroamphetamine / Q000008:administration & dosage* / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006220:Haloperidol / Q000494:pharmacology; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D009714:Nucleus Accumbens / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012653:Self Stimulation
D015102:3,4-Dihydroxyphenylacetic Acid; D003366:Cosyntropin; D000324:Adrenocorticotropic Hormone; D006220:Haloperidol; D001058:Apomorphine; D003913:Dextroamphetamine; D004298:Dopamine; D006719:Homovanillic Acid