Crowder J M, Norris D K, Bradford H F
Biochem Pharmacol. 1986 Aug 1;35(15):2501-7. doi: 10.1016/0006-2952(86)90046-8.
Morphine (1-100 microM) was found to inhibit several concomitant events in brain slices and synaptosomes which are augmented by depolarizing agents. Thus, 45Ca2+ uptake, amino acid neurotransmitter release, increases in 3',5' cyclic AMP levels and 32Pi incorporation to proteins and lipids induced by veratrine (25 microM) and by potassium (56 mM), were each inhibited in a dose related manner. These inhibitory actions of morphine were all prevented by naloxone (1 microM). Evidence is presented that morphine binding to a receptor on the synaptic membrane affects intracellular mechanisms involved in neurotransmitter release possibly via a second messenger system. An enhancing action of GTP on the inhibitory influences of morphine suggests that its actions are mediated at least in part, via a coupling of the receptor to adenyl cyclase in the outer membrane. This is supported by its inhibitory action on the capacity of depolarizing agents to increase cyclic AMP levels.
研究发现，吗啡（1 - 100微摩尔）可抑制脑片和突触体中的几种伴随事件，而这些事件会因去极化剂而增强。因此，由藜芦碱（25微摩尔）和钾（56毫摩尔）诱导的45Ca2+摄取、氨基酸神经递质释放、3',5'环磷酸腺苷水平升高以及32Pi掺入蛋白质和脂质，均以剂量相关的方式受到抑制。纳洛酮（1微摩尔）可完全阻止吗啡的这些抑制作用。有证据表明，吗啡与突触膜上的受体结合可能通过第二信使系统影响参与神经递质释放的细胞内机制。鸟苷三磷酸（GTP）对吗啡抑制作用的增强作用表明，其作用至少部分是通过受体与外膜腺苷酸环化酶的偶联介导的。这一点得到了其对去极化剂增加环磷酸腺苷水平能力的抑制作用的支持。
