Possible role of dopamine in diethylstilbestrol-elicited accumulation of cyclic AMP in incubated male rat hypothalamus.
Pimozide and haloperidol, the dopaminergic antagonists, have been shown to effectively block diethylstilbestrol (DES)-elicited [3H] adenosine 3', 5'-monophosphate (cAMP) accumulation in incubated hypothalami from immature male rats. Several noradrenergic antagonists (i.e. propranolol, MJ-1999 and phenoxybenzamine) failed to reduce [3H]cAMP levels significantly. Pimozide was found to be more specific than haloperidol as it did not effect norepinephrine (NE)-elicited formation of [3H]cAMP, while the latter blocker caused a 48% reduction of the stimulation by NE. Pimozide was also more potent than haloperidol in inhibiting DES-stimulated [3H]cAMP formation. It can be inferred from these data that as a result of DES-receptor interaction dopamine (DA) is released and in turn activates DA-sensitive adenylate cyclase in the hypothalamus.
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D004054:Diethylstilbestrol / Q000494:pharmacology*; D004298:Dopamine / Q000494:pharmacology; D018492:Dopamine Antagonists; D006220:Haloperidol / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects* / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D010643:Phenoxybenzamine / Q000494:pharmacology; D010868:Pimozide / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats
D018492:Dopamine Antagonists; D010643:Phenoxybenzamine; D010868:Pimozide; D004054:Diethylstilbestrol; D011433:Propranolol; D000242:Cyclic AMP; D006220:Haloperidol; D004298:Dopamine; D009638:Norepinephrine