Regulation of adenylate cyclase activity mediated by muscarinic acetylcholine receptors.
Regulation of adenylate cyclase activity mediated by muscarinic acetylcholine receptors.
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由毒蕈碱乙酰胆碱受体介导的腺苷酸环化酶活性的调节。
DOI：
10.1073/pnas.75.4.1788
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发表时间：
1978
影响因子：
11.1
通讯作者：
M. Nirenberg
中科院分区：
文献类型：
--
作者：
N. Nathanson;W. Klein;M. Nirenberg
Carbachol是NG108-15杂交细胞毒蕈碱乙酰胆碱受体的激活剂，它能快速、可逆地抑制腺苷酸环化酶[ATP焦磷酸盐裂解酶（环化），EC 4.6.1.1]，并在24-30小时内缓慢地引起腺苷酸环化酶活性增加200-300%。腺苷酸环化酶的抑制和酶活性的逐渐增加都依赖于毒蕈碱乙酰胆碱受体和受体激活剂。停药后腺苷酸环化酶活性在6小时内逐渐恢复到控制水平；酶活性衰减的半衰期为1.6小时。这些结果表明，毒蕈碱乙酰胆碱受体介导腺苷酸环化酶活性的短暂和长期影响，类似于阿片类药物。
Carbachol, an activator of muscarinic acetylcholine receptors of NG108-15 hybrid cells, inhibits adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] rapidly and reversibly and slowly evokes a 200-300% increase in adenylate cyclase activity over a period of 24-30 hr. Both the inhibition of adenylate cyclase and the gradual increase in enzyme activity are dependent on muscarinic acetylcholine receptors and the receptor activator. Withdrawal of carbachol results in a gradual return of adenylate cyclase activity to control levels over a period of 6 hr; the half-life for decay of enzyme activity is 1.6 hr. These results show that muscarinic acetylcholine receptors mediate both transient and long-lived effects on adenylate cyclase activity that resemble those of opiates.