Tsunoo A, Narahashi T
Brain Res. 1984 Feb 27;294(1):123-6. doi: 10.1016/0006-8993(84)91315-5.
Adenosine, 2-chloroadenosine and prostaglandin E1 which are known to increase cyclic AMP in neuroblastoma cells potentiated the acetylcholine-induced muscarinic hyperpolarization of the cells without changing the resting membrane potential. The potentiation caused by 2-chloroadenosine was further augmented by Ro 20-1724, a phosphodiesterase inhibitor. A direct intracellular pressure application of cyclic AMP potentiated the muscarinic hyperpolarization without changing the resting membrane potential. Morphine which inhibits adenylate cyclase antagonized 2-chloroadenosine-induced potentiation of the muscarinic hyperpolarization. These results suggest that changes in cyclic AMP level modulate the muscarinic response of neuroblastoma cells.
已知可增加神经母细胞瘤细胞中环磷酸腺苷(cAMP)的腺苷、2-氯腺苷和前列腺素E1,在不改变静息膜电位的情况下,增强了乙酰胆碱诱导的细胞毒蕈碱超极化。磷酸二酯酶抑制剂Ro 20-1724进一步增强了2-氯腺苷引起的增强作用。直接向细胞内施加cAMP可增强毒蕈碱超极化,而不改变静息膜电位。抑制腺苷酸环化酶的吗啡可拮抗2-氯腺苷诱导的毒蕈碱超极化增强作用。这些结果表明,cAMP水平的变化调节神经母细胞瘤细胞的毒蕈碱反应。