Vanecek J
Institute of Physiology, Academy of Sciences of Czech Republic, Prague.
Mol Cell Endocrinol. 1995 Feb;107(2):149-53. doi: 10.1016/0303-7207(94)03437-x.
In neonatal rat pituitary, melatonin inhibits GnRH-induced increase of cAMP and [Ca2+]i. Both effects are transduced by specific high-affinity melatonin receptors coupled with pertussis toxin-sensitive G-protein. We have attempted to determine whether melatonin acts via independent pathways on both messengers or whether the indole directly inhibits only one of the messengers and the second is decreased as a secondary consequence. Melatonin inhibition of cAMP accumulation was not prevented by agents known to block melatonin effect on [Ca2+]i such as Na(+)- or Ca2(+)-free medium, Bay K, nifedipine, KCl or gramicidin. Melatonin effect on [Ca2+]i was not prevented by forskolin or 8-bromo-cAMP. We therefore conclude that melatonin inhibits cAMP accumulation and [Ca2+]i increase independently by separate pathways.
在新生大鼠垂体中，褪黑素抑制促性腺激素释放激素（GnRH）诱导的环磷酸腺苷（cAMP）和细胞内钙离子浓度（[Ca2+]i）的升高。这两种效应均由与百日咳毒素敏感的G蛋白偶联的特异性高亲和力褪黑素受体介导。我们试图确定褪黑素是通过独立的途径作用于这两种信使分子，还是该吲哚仅直接抑制其中一种信使分子，而另一种则作为次要结果而降低。已知能阻断褪黑素对[Ca2+]i作用的试剂，如无钠或无钙培养基、Bay K、硝苯地平、氯化钾或短杆菌肽，不能阻止褪黑素对cAMP积累的抑制作用。福斯可林或8-溴-cAMP不能阻止褪黑素对[Ca2+]i的作用。因此，我们得出结论，褪黑素通过独立的途径分别抑制cAMP积累和[Ca2+]i升高。
