Dopamine inhibition of neurotensin-induced increase in Ca2+ influx into rat pituitary cells.
In this paper, we report that the intracellular mechanism by which neurotensin stimulates prolactin release involves an increase in Ca2+ uptake by pituitary cells rather than an effect on adenylate cyclase system. In addition, dopamine can prevent neurotensin-induced calcium influx by interacting with dopamine D2-receptors which appear to be completely independent of the adenylate cyclase moiety but are coupled to calcium channels.
Memo
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M
Carboni
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Trabucchi
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Carruba
M O
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Spano
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D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001971:Bromocriptine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D004298:Dopamine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D009496:Neurotensin / Q000494:pharmacology*; D010902:Pituitary Gland / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000378:metabolism
D007473:Ion Channels; D011954:Receptors, Dopamine; D009496:Neurotensin; D001971:Bromocriptine; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D001058:Apomorphine; D002118:Calcium; D004298:Dopamine