Steele T D, Nichols D E, Yim G K
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907.
Pharmacol Biochem Behav. 1989 Oct;34(2):223-7. doi: 10.1016/0091-3057(89)90303-1.
(+-)-3,4-Methylenedioxymethamphetamine (MDMA) (10, 20, and 40 mg/kg) was administered to male CF-1 mice which were sacrificed 3, 6, or 24 hours posttreatment for analysis of brain and cardiac biogenic amines and metabolites. In contrast to reported effects of MDMA in the rat, the highest dose of MDMA transiently elevated mouse brain 5-hydroxytryptamine (5-HT) 3 hours following drug treatment. Levels of dopamine were not significantly affected. 5-Hydroxyindoleacetic acid and dihydroxyphenylacetic acid were significantly lowered by MDMA at the two early time points. The highest dose of MDMA produced a transient depletion of norepinephrine in mouse brain and heart tissue. Only the effects of MDMA on cardiac norepinephrine were prevented by pretreatment of animals with desipramine. A regimen consisting of four daily doses of 40 mg/kg MDMA only produced significant declines in 5-HIAA, dopamine and homovanillic acid levels one week following the last dose. These data confirm previous reports that mice are resistant to the neurotoxic effects of MDMA suggesting that a species variation in response to MDMA exists.
将（±）-3,4-亚甲基二氧甲基苯丙胺（摇头丸）（10、20和40毫克/千克）给予雄性CF-1小鼠，在治疗后3、6或24小时处死，以分析脑和心脏生物胺及代谢产物。与报道的摇头丸对大鼠的作用相反，最高剂量的摇头丸在药物治疗后3小时使小鼠脑5-羟色胺（5-HT）短暂升高。多巴胺水平未受到显著影响。在两个早期时间点，5-羟吲哚乙酸和二羟基苯乙酸被摇头丸显著降低。最高剂量的摇头丸使小鼠脑和心脏组织中的去甲肾上腺素短暂耗竭。只有通过用去甲丙咪嗪预处理动物才能阻止摇头丸对心脏去甲肾上腺素的作用。由每日40毫克/千克摇头丸的四个剂量组成的方案仅在最后一剂后一周使5-羟吲哚乙酸、多巴胺和高香草酸水平显著下降。这些数据证实了先前的报道，即小鼠对摇头丸的神经毒性作用具有抗性，表明存在对摇头丸反应的物种差异。
