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单胺受体拮抗剂对大鼠尼古丁诱导的食欲减退的影响。

Effects of monoamine receptor antagonists on nicotine-induced hypophagia in the rat.

作者信息

Zarrindast M R, Oveisi M R

机构信息

Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Iran.

出版信息

Eur J Pharmacol. 1997 Feb 26;321(2):157-62. doi: 10.1016/s0014-2999(96)00935-1.

DOI:10.1016/s0014-2999(96)00935-1
PMID:9063683
Abstract

(--)-Nicotine, in doses of 0.2-0.6 mg/kg intraperitoneally (i.p.), induced a dose-dependent anorexia 1 h, 2 h and 4 h after food presentation in 20-h food-restricted male rats. The anorectic response of nicotine (0.4 mg/kg, 30 min before the test) was prevented by pretreatment with the central nicotine receptor antagonist mecamylamine (0.5 and 1 mg/kg). The peripheral nicotine receptor antagonist hexamethonium (5 and 10 mg/kg), the muscarinic receptor antagonist atropine (5 and 10 mg/kg), the dopamine D2 receptor antagonist pimozide (0.5 and 1 mg/kg), the dopamine D1 receptor antagonist SCH23390 (R-(+)-8-chloro-2, 3, 4, 5-tetrahydro-3-methyl-5-phenyl-1 H-3-benzazepine-7ol maleate; 0.05 and 0.1 mg/kg), the alpha-adrenoceptor antagonist phenoxybenzamine (5 and 10 mg/kg), and the beta-adrenoceptor antagonist propranolol (5 and 10 mg/kg) amplified the nicotine response while promoting anorexia by themselves. The dopamine D2 receptor antagonist sulpiride (25, 50 and 100 mg/kg) increased food intake and amplified the anorectic effect of nicotine. The 5-HT receptor antagonists metergoline (0.5 and 1 mg/kg) and mianserin (1 and 2 mg/kg) increased the nicotine effect. When the antagonists were used alone, metergoline did not change food intake, while mianserin increased food intake. It can be concluded that part of nicotine-induced anorexia is mediated through central nicotinic receptors.

摘要

在20小时食物受限的雄性大鼠中,腹腔注射(i.p.)剂量为0.2 - 0.6毫克/千克的(-)-尼古丁,在食物呈现后1小时、2小时和4小时会引起剂量依赖性的厌食。尼古丁(0.4毫克/千克,测试前30分钟)的厌食反应可通过中枢尼古丁受体拮抗剂美加明(0.5和1毫克/千克)预处理来预防。外周尼古丁受体拮抗剂六甲铵(5和10毫克/千克)、毒蕈碱受体拮抗剂阿托品(5和10毫克/千克)、多巴胺D2受体拮抗剂匹莫齐特(0.5和1毫克/千克)、多巴胺D1受体拮抗剂SCH23390(R-(+)-8-氯-2,3,4,5-四氢-3-甲基-5-苯基-1H-3-苯并氮杂卓-7醇马来酸盐;0.05和0.1毫克/千克)、α-肾上腺素能受体拮抗剂酚苄明(5和10毫克/千克)以及β-肾上腺素能受体拮抗剂普萘洛尔(5和10毫克/千克)在自身促进厌食的同时会增强尼古丁反应。多巴胺D2受体拮抗剂舒必利(25、50和100毫克/千克)增加食物摄入量并增强尼古丁的厌食作用。5-羟色胺受体拮抗剂美替拉酮(0.5和1毫克/千克)和米安色林(1和2毫克/千克)增强尼古丁的作用。当单独使用拮抗剂时,美替拉酮不改变食物摄入量,而米安色林增加食物摄入量。可以得出结论,尼古丁诱导的厌食部分是通过中枢烟碱受体介导的。

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