Beleslin D B, Krstić S K
Physiol Behav. 1987;39(6):681-6. doi: 10.1016/0031-9384(87)90250-2.
In unanesthetized cats the emetic action of an injection of nicotine into the cerebral ventricle through chronically implanted cannulae was investigated. Nicotine injected in doses of 0.02-1.0 mg produced dose-dependent vomiting, which was abolished after ablation of the area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. The emetic response to intracerebroventricular (ICV) nicotine as well as the vomiting produced by intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. On the other hand, the emetic response to ICV nicotine and to intragastric copper sulfate was virtually unchanged in cats pretreated with ICV 6-hydroxydopamine and 5,6-dihydroxytryptamine. The duration of vomiting produced by intragastric copper sulfate, but not that of ICV nicotine, was potentiated in cats pretreated with hemicholinium-3. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV nicotine. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic receptor antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine antagonist all injected into the cerebral ventricle had virtually no effect on the vomiting induced by ICV nicotine. It is postulated that nicotine evokes vomiting by its action on nicotinic receptors within the area postrema but not on catecholaminergic or serotonergic neurones. Finally, acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.
在未麻醉的猫身上，研究了通过长期植入的套管向脑室注射尼古丁的催吐作用。注射剂量为0.02 - 1.0毫克的尼古丁会产生剂量依赖性呕吐，在损毁最后区后呕吐消失。然而，胃内给予硫酸铜会使最后区被损毁的猫发生呕吐。预先经脑室内（ICV）给予利血平的猫，对脑室内尼古丁的催吐反应以及胃内硫酸铜引起的呕吐会受到抑制或消失。另一方面，预先经脑室内给予6 - 羟基多巴胺和5,6 - 二羟基色胺的猫，对脑室内尼古丁和胃内硫酸铜的催吐反应基本未变。预先给予半胱胺酸 - 3的猫，胃内硫酸铜引起的呕吐持续时间延长，但脑室内尼古丁引起的呕吐持续时间未变。脑室内注射神经节阻断剂美加明和六甲铵可防止脑室内尼古丁引起的呕吐。另一方面，向脑室内注射的多种抗毒蕈碱药物、α和β肾上腺素能受体拮抗剂、多巴胺拮抗剂、抗组胺药和5 - 羟色胺拮抗剂对脑室内尼古丁引起的呕吐几乎没有影响。据推测，尼古丁通过作用于最后区内的烟碱受体而非儿茶酚胺能或5 - 羟色胺能神经元来引发呕吐。最后，乙酰胆碱也可能参与抑制呕吐中枢调节的复杂机制。
