| pubmed-article:2415214 | pubmed:abstractText | 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. | lld:pubmed |
