Mechanism(s) by which the transient removal of dopamine regulation potentiates the prolactin-releasing action of thyrotropin-releasing hormone.
Mechanism(s) by which the transient removal of dopamine regulation potentiates the prolactin-releasing action of thyrotropin-releasing hormone.
复制标题
短暂消除多巴胺调节可增强促甲状腺素释放激素的催乳素释放作用的机制。
作者：
G. Martínez de la Escalera;R. Weiner
多巴胺（DA）的瞬时清除选择性地增强促甲状腺激素释放激素（TRH）的催乳素（PRL）释放作用，但不增强血管活性肠肽（VIP）。与这些研究结果一致，激活Ca 2 +/蛋白激酶C第二信使途径但不激活腺苷酸环化酶系统的药物的PRL刺激作用也得到加强。在目前的研究中，我们已经扩展了这些发现，以确定第二信使系统介导的增强行动的DA的去除。分散的垂体前叶细胞E2处理的SD大鼠培养在塑料盖玻片。用DA（500 nM）进行张力灌注的细胞在没有额外处理或用8-Br-环腺苷一磷酸（8-Br-cAMP）、Ca 2+离子载体A23187、12-O-十四烷酰基-佛波醇-13-乙酸酯（TPA）、TRH或VIP处理10分钟后20分钟用TRH（100 nM）进行攻击。TRH反应的增强与在去除DA 10分钟后观察到的4至5倍增强相比，所用浓度（500 μ M）的8-Br-cAMP不能改变PRL释放的基础速率，但是，作为VIP（500 nM），增强TRH的PRL释放作用2至3倍。TRH（100 nM）的预先给药不影响细胞对20分钟后用TRH的第二次攻击的反应性。A23187（20 μ M）和TPA（5或50 nM）均诱导PRL释放速率持续升高。TPA处理的细胞表现出对TRH的反应性增加，而A23187处理的细胞没有。（250字处删节）
The transient removal of dopamine (DA) selectively potentiated the prolactin (PRL) releasing action of thyrotropin-releasing hormone (TRH) but not vasoactive intestinal peptide (VIP). Consistent with these findings, the PRL-stimulating actions of agents which activated the Ca2+/protein kinase C second messenger pathway but not the adenylate cyclase system were also potentiated. In the current study we have extended these findings to determine the second messenger system mediating the potentiating action of the removal of DA. Dispersed anterior pituitary cells from E2-treated Sprague-Dawley rats were cultured on plastic coverslips. Cells tonically superfused with DA (500 nM were challenged with TRH (100 nM) 20 min after no additional treatment or a 10-min treatment with 8-Br-cyclic adenosine monophosphate (8-Br-cAMP), the Ca2+ ionophore A23187,12-O-tetradecanoyl-phorbol-13-acetate (TPA), TRH, or VIP. The potentiation of the TRH response was compared to the 4- to 5-fold potentiation observed following the removal of DA for 10 min 8-Br-cAMP at the concentration used (500 microM) was unable to alter the basal rate of PRL release, but, as VIP (500 nM), potentiated 2- to 3-fold the PRL-releasing action of TRH. A prior administration of TRH (100 nM) did not affect the responsiveness of the cells to a second challenge with TRH 20 min later. Both A23187 (20 microM) and TPA (5 or 50 nM) induced a sustained rise in the rate of PRL release. TPA-treated cells showed an increased responsiveness to TRH, whereas A23187-treated cells did not.(ABSTRACT TRUNCATED AT 250 WORDS)