Guérineau N C, Lledo P M, Verrier D, Israel J M
Laboratoire de Neurophysiologie, URA CNRS 1200, Université de Bordeaux, France.
Cell Biol Toxicol. 1994 Dec;10(5-6):311-6. doi: 10.1007/BF00755776.
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.
在培养的正常大鼠催乳素细胞（轻组分和重组分）的两个群体中，测量了催乳素（PRL）释放和细胞内游离钙浓度[Ca2+]i。与轻组分催乳素细胞相比，重组分细胞的自发性PRL释放对二氢吡啶类药物（DHPs；Bay K 8644和硝苯地平）更敏感。促甲状腺激素释放激素（TRH）对重组分细胞PRL释放的刺激作用被Cd2+抑制，并被Bay K 8644模拟。Indo-1实验表明，TRH升高的[Ca2+]i被Cd2+可逆性抑制。在不含钙的含EGTA培养基中，TRH不改变[Ca2+]i。
