Capuzzo A, Borasio P G, Fabbri E
Institute of General Physiology, University of Ferrara, Italy.
Neurochem Res. 1988 Nov;13(11):1049-53. doi: 10.1007/BF00973149.
There is considerable evidence that adenosine 3',5'-cyclic monophosphate (cAMP) is involved in the modulation of synaptic transmission in the guinea pig superior cervical ganglion (SCG). Presynaptic muscarinic receptors are known to attenuate, when activated, acetylcholine (ACh) release in the periphery as well as in the brain. Thus, the possible relationship between ganglionic adenylate cyclase activity and the output of ACh from electrically stimulated ganglia, preloaded with [3H]choline, was investigated. The muscarinic agonist oxotremorine significantly reduced in a dose-dependent manner the electrically evoked neurotransmitter release. The adenylate cyclase inhibitor N-(cis-2-phenylcyclopentyl)azacyclotridecan-2-imine hydrochloride (RMI 12330 A) also decreased ACh output. The inhibitory effects of these two drugs were additive. In crude ganglion membrane fractions oxotremorine significantly inhibited adenylate cyclase activity. The results indicate that drugs capable of inhibiting adenylate cyclase, significantly decrease ACh output from preganglionic nerve terminals in guinea pig SCG.
有大量证据表明，3',5'-环磷酸腺苷（cAMP）参与豚鼠颈上神经节（SCG）突触传递的调节。已知突触前毒蕈碱受体被激活时会减弱外周以及大脑中乙酰胆碱（ACh）的释放。因此，研究了神经节腺苷酸环化酶活性与预先加载[3H]胆碱的电刺激神经节中ACh输出之间的可能关系。毒蕈碱激动剂氧化震颤素以剂量依赖性方式显著降低电诱发的神经递质释放。腺苷酸环化酶抑制剂N-（顺式-2-苯基环戊基）氮杂环十三烷-2-亚胺盐酸盐（RMI 12330 A）也降低了ACh输出。这两种药物的抑制作用是相加的。在粗制神经节膜组分中，氧化震颤素显著抑制腺苷酸环化酶活性。结果表明，能够抑制腺苷酸环化酶的药物会显著降低豚鼠SCG节前神经末梢的ACh输出。
