Catalepsy, hypermotility, increase of striatal acetylcholine release induced by morphine and Met-enkephalin as affected by prolonged hydrocortisone and ACTH treatment.
In the rats treated with ACTH or hydrocortisone for 14 days the catalepsy induced by morphine was almost completely inhibited, while the haloperidol induced catalepsy remained unchanged. The morphine induced hypermotility was altered neither by prolonged treatment with ACTH nor by an acute glucocorticoid administration. Inhibition of Na/K ATPase by ouabain led to an increase of striatal acetylcholine (Ach) release, which was enhanced by Met-enkephalin. This effect of the opioid peptide was not demonstrable in the striata of ACTH or hydrocortisone pretreated rats. It is concluded that glucocorticoids are regulatory factors of the striatal opiate neurotransmission possibly via altered receptorial mechanisms.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D002375:Catalepsy / Q000139:chemically induced / Q000517:prevention & control; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004744:Enkephalin, Methionine / Q000494:pharmacology*; D006220:Haloperidol / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009043:Motor Activity / Q000187:drug effects; D051381:Rats
D004744:Enkephalin, Methionine; D009020:Morphine; D000324:Adrenocorticotropic Hormone; D006220:Haloperidol; D006854:Hydrocortisone