Ueda H, Tamura S, Harada H, Yasumoto T, Takagi H
Neurosci Lett. 1986 Jun 18;67(2):141-6. doi: 10.1016/0304-3940(86)90387-3.
Effects of the Gs protein-mediated adenylate cyclase facilitatory system on Ca2+ entry into synaptosomes were studied, using two specific toxins. A putative Ca2+-channel agonist, maitotoxin (MTX), increased the 45Ca2+ entry and [Ca2+]i, determined with Quin-II, into synaptosomes of the rat brainstem, which were not attenuated by nifedipine. However, another Ca2+-channel agonist, BAY K-8644 did not alter the 45Ca2+ entry nor [Ca2+]i. The MTX-induced increase of the 45Ca2+ entry was significantly enhanced by addition of dibutyryl cyclic adenosine monophosphate and by the pretreatment with cholera toxin. These findings support the view that stimulation of presynaptic receptors coupled to the Gs-adenylate cyclase system may lead to a facilitation of the release of neurotransmitters, through a cAMP dependent enhancement of the opening of the Ca2+ channels located on nerve terminals.
利用两种特异性毒素研究了Gs蛋白介导的腺苷酸环化酶促进系统对Ca2+进入突触体的影响。一种假定的Ca2+通道激动剂，刺尾鱼毒素（MTX），增加了用喹啉-II测定的大鼠脑干突触体中45Ca2+的进入和[Ca2+]i，而硝苯地平对此无减弱作用。然而，另一种Ca2+通道激动剂，BAY K-8644并未改变45Ca2+的进入或[Ca2+]i。添加二丁酰环磷酸腺苷和用霍乱毒素预处理可显著增强MTX诱导的45Ca2+进入增加。这些发现支持这样一种观点，即与Gs-腺苷酸环化酶系统偶联的突触前受体的刺激可能通过cAMP依赖性增强神经末梢上Ca2+通道的开放而导致神经递质释放的促进。
