Possible role of prolactin in the modification of medial basal hypothalamic glutamic acid decarboxylase activity.
The effects of acute and chronic injections of haloperidol, sulpiride and apomorphine on serum prolactin (PRL) levels and medial basal hypothalamus (MBH) glutamic acid decarboxylase (GAD) activity were investigated in male rats. Parallel changes in PRL and GAD activity were observed in acutely treated animals. Conversely, a return to normal of the GAD activity associated with high plasma PRL levels was induced by chronic haloperidol and sulpiride treatment. Results are discussed in the light of the possible existence of a hypothetical PRL-gamma-aminobutyric acid (GABA) subsidiary feedback loop.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002262:Carboxy-Lyases / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D011388:Prolactin / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D013469:Sulpiride / Q000494:pharmacology
D013469:Sulpiride; D011388:Prolactin; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D006220:Haloperidol; D001058:Apomorphine