Evidence that TRH controls prolactin release from rat lactotrophs by stimulating a calcium influx

Prolactin (PRL) release and intracellular free calcium concentration [Ca2+]i were measured in two populations of normal rat lactotrophs (light and heavy fractions) in culture. Spontaneous PRL release of heavy fraction cells was more sensitive to dihydropyridines (DHPs; Bay K 8644 and nifedipine) when compared to the light fraction lactotrophs. The stimulatory effect of thyrotropin-releasing hormone (TRH) on PRL release from heavy fraction cells was inhibited by Cd2+ and mimicked by Bay K 8644. Indo-1 experiments revealed that TRH-increased [Ca2+]i was reversibly inhibited by Cd2+. In a Ca(2+)-free EGTA-containing medium, TRH did not modify [Ca2+]i.