Judd A M, MacLeod R M
Department of Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
Eur J Pharmacol. 1991 Mar 19;195(1):101-6. doi: 10.1016/0014-2999(91)90386-5.
MMQ cells, a prolactin-secreting cell line possessing dopamine receptors, were exposed to the calcium channel activator maitotoxin and dopamine or adrenoceptor agonists or antagonists. Dopamine (500 nM) or the dopamine agonists lisuride (50 nM), terguride (50 nM), and N-0437 (50 nM) decreased maitotoxin-stimulated prolactin release from perifused MMQ cells. In this system, sulpiride (100 nM), a dopamine D2 antagonist, reversed the prolactin inhibition produced by lisuride (20 nM). In static incubations of MMQ cells, lisuride (10-500 nM) inhibited maitotoxin-stimulated prolactin release in a concentration-dependent manner; this inhibition was attenuated in a concentration-related manner by sulpiride (100-500 nM). In addition, sulpiride reversed dopamine (50-500 nM), lisuride (10-500 nM), and terguride (50-500 nM) inhibition of forskolin-stimulated cAMP generation. The alpha 2-adrenergic agonist clonidine inhibited maitotoxin-stimulated prolactin release from perifused MMQ cells; this inhibition was abolished by idazoxan, an alpha 2-adrenergic antagonist. In contrast, serotonin or the serotonin antagonist methysergide had no effect on prolactin release from MMQ cells. These data indicate that activation of dopamine D2 receptors and alpha 2-adrenoceptors by classically defined pharmacological agents inhibits prolactin release and cellular cAMP levels in MMQ cells. Therefore, MMQ cells may provide a valuable model for the development of pharmacological agents and assist in the identification of the mechanisms involved in the dopaminergic inhibition of prolactin release.
MMQ细胞是一种具有多巴胺受体的分泌催乳素的细胞系，将其暴露于钙通道激活剂 maitotoxin 以及多巴胺或肾上腺素能受体激动剂或拮抗剂中。多巴胺（500 nM）或多巴胺激动剂利舒脲（50 nM）、替古瑞肽（50 nM）和N - 0437（50 nM）可降低从灌流的MMQ细胞中由 maitotoxin 刺激引起的催乳素释放。在该系统中，多巴胺D2拮抗剂舒必利（100 nM）可逆转利舒脲（20 nM）对催乳素的抑制作用。在MMQ细胞的静态培养中，利舒脲（10 - 500 nM）以浓度依赖性方式抑制由 maitotoxin 刺激引起的催乳素释放；舒必利（100 - 500 nM）以浓度相关方式减弱这种抑制作用。此外，舒必利可逆转多巴胺（50 - 500 nM）、利舒脲（10 - 500 nM）和替古瑞肽（50 - 500 nM）对福司可林刺激的cAMP生成的抑制作用。α2 - 肾上腺素能激动剂可乐定抑制从灌流的MMQ细胞中由 maitotoxin 刺激引起的催乳素释放；这种抑制作用被α2 - 肾上腺素能拮抗剂咪唑克生消除。相反，5 - 羟色胺或5 - 羟色胺拮抗剂甲基麦角新碱对MMQ细胞的催乳素释放没有影响。这些数据表明，经典定义的药理剂激活多巴胺D2受体和α2 - 肾上腺素能受体可抑制MMQ细胞中的催乳素释放和细胞cAMP水平。因此，MMQ细胞可能为药理剂的开发提供有价值的模型，并有助于确定多巴胺能抑制催乳素释放所涉及的机制。
