Ohmichi M, Hirota K, Koike K, Kadowaki K, Yamaguchi M, Miyake A, Tanizawa O
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Neuroendocrinology. 1990 Jul;52(1):75-81. doi: 10.1159/000125542.
Coupling of the dopamine (DA) receptor to the pathway of arachidonate (AA) through the islet-activating protein (IAP)-sensitive GTP-binding (G) protein was examined in primary cultures of anterior pituitary cells. The inhibitions by 1 microM DA of the stimulations of prolactin (PRL) release by 100 nM thyrotropin-releasing hormone and by 10 microM calcium ionophore A23187 were blocked by 100 ng/ml IAP. DA at 1 microM did not inhibit the release of [3H]-AA induced by 100 mU/ml phospholipase A2 (PLA2), but it inhibited the release of PRL induced by 100 mU/ml PLA2. This inhibition was blocked by 100 ng/ml IAP. IAP also blocked the inhibitions by DA of the releases of PRL by 5 microM AA and by 5 microM 5-hydroxyeicosatetraenoic acid. These results suggest that the DA receptor on lactotrophs is coupled to the pathway following the release of AA (lipoxygenase) through the IAP-sensitive G protein.
在垂体前叶细胞原代培养物中研究了多巴胺(DA)受体通过对百日咳毒素(IAP)敏感的鸟苷三磷酸结合(G)蛋白与花生四烯酸(AA)途径的偶联。1微摩尔DA对100纳摩尔促甲状腺激素释放激素和10微摩尔钙离子载体A23187刺激催乳素(PRL)释放的抑制作用被100纳克/毫升IAP阻断。1微摩尔DA不抑制100毫单位/毫升磷脂酶A2(PLA2)诱导的[3H]-AA释放,但它抑制100毫单位/毫升PLA2诱导的PRL释放。这种抑制作用被100纳克/毫升IAP阻断。IAP也阻断了DA对5微摩尔AA和5微摩尔5-羟基二十碳四烯酸诱导的PRL释放的抑制作用。这些结果表明,泌乳细胞上的DA受体通过对IAP敏感的G蛋白与AA释放后(脂氧合酶)的途径偶联。