Richardson J S, Mattio T G, Giacobini E
Can J Physiol Pharmacol. 1984 Jul;62(7):857-9. doi: 10.1139/y84-143.
The electrically stimulated release of [3H]acetylcholine from the parasympathetic nerve terminals of the rat iris in vitro is increased in a dose-dependent manner by scopolamine but is decreased by the tricyclic antidepressants amitriptyline and imipramine. The increased release in the presence of scopolamine seems to be due to the blockade of a presynaptic muscarinic autoreceptor that, in the drug-free state, inhibits the release of acetylcholine. However, at drug concentrations that should have comparable antimuscarinic potency, the antidepressants inhibit the release of acetylcholine. This suggests that the anticholinergic side effects of the antidepressants may be due to the reduced release of acetylcholine from parasympathetic nerve terminals as well as a possible direct postsynaptic muscarinic receptor blocking action. Whatever the mechanism of this action, the antidepressants do not have the same effect as scopolamine at the presynaptic muscarinic autoreceptor in the rat iris.
在体外，东莨菪碱可使大鼠虹膜副交感神经末梢释放的[3H]乙酰胆碱经电刺激后呈剂量依赖性增加，而三环类抗抑郁药阿米替林和丙咪嗪则使其减少。东莨菪碱存在时释放增加似乎是由于突触前毒蕈碱自身受体被阻断，在无药物状态下，该受体抑制乙酰胆碱的释放。然而，在具有相当抗毒蕈碱效力的药物浓度下，抗抑郁药却抑制乙酰胆碱的释放。这表明抗抑郁药的抗胆碱能副作用可能是由于副交感神经末梢乙酰胆碱释放减少以及可能的直接突触后毒蕈碱受体阻断作用。无论这种作用机制如何，抗抑郁药在大鼠虹膜突触前毒蕈碱自身受体上的作用与东莨菪碱不同。
