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Evidence that TRH controls prolactin release from rat lactotrophs by stimulating a calcium influx
Authors:N C Guérineau  P M Lledo  D Verrier  J M Israel
Institution:(1) Laboratoire de Neurophysiologie, URA CNRS 1200, Université de Bordeaux 2, 33076 Bordeaux Cédex, France;(2) Institut A. Fessard, CNRS UPR 2212, 91198 Gif/Yvette, France;(3) INSERM 394, rue C. Saint Saëns, 33077 Bordeaux Cédex, France;(4) INSERM U 378, Université de Bordeaux 2, rue Léo Saignat, 33076 Bordeaux, France
Abstract: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 Ca2+-free EGTA-containing medium, TRH did not modify Ca2+]i.Abbreviations Ca2+]i intracellular free calcium concentration - DA dopamine - DHP dihydropyridine(s) - DMEM Dulbecco's Modified Eagle's Medium - Ins(1,4,5)P3 inositol 1,4,5-trisphosphate - PRL prolactin - RIA radioimmunoassay - TRH thyrotropin-releasing hormone - VGCC voltage-gated calcium channel
Keywords:calcium  dihydropyridine  lactotroph  TRH
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