Suppr超能文献

3,4-亚甲二氧基乙胺(MDEA,“伊芙”)对大鼠体温的急性影响以及脑中5-羟色胺能神经元的长期变性:与3,4-亚甲二氧基甲基苯丙胺(“摇头丸”)的比较

The acute effect in rats of 3,4-methylenedioxyethamphetamine (MDEA, "eve") on body temperature and long term degeneration of 5-HT neurones in brain: a comparison with MDMA ("ecstasy").

作者信息

Colado M I, Granados R, O'Shea E, Esteban B, Green A R

机构信息

Department of Pharmacology, Faculty of Medicine, Complutense University, Madrid, Spain.

出版信息

Pharmacol Toxicol. 1999 Jun;84(6):261-6. doi: 10.1111/j.1600-0773.1999.tb01492.x.

Abstract

Administration of a single dose of the recreationally used drug 3,4-methylenedioxyethamphetamine (MDEA or "eve") to Dark Agouti rats resulted in an acute dose-dependent hyperthermic response. The peak effect and duration of hyperthermia of a dose of MDEA of 35 mg/kg intraperitoneally was similar to a dose of 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") of 15 mg/kg intraperitoneally. Seven days later this dose of MDMA produced a marked (approximately 50%) loss of 5-HT and its metabolite 5-HIAA in cortex, hippocampus and striatum and a similar loss of [3H]-paroxetine binding in cortex: these losses reflecting the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. In contrast, administration of MDEA (15, 25 or 35 mg/kg), even at the highest dose, produced only a 20% loss in cortex and hippocampus and no decrease in striatum. The neurotoxic effect of MDEA was only weakly dose-dependent. Neither MDEA (35 mg/kg) nor MDMA (15 mg/kg) altered striatal dopamine content 7 days later. MDEA appeared to have about half the potency of MDMA in inducing acute hyperthermia and 25% of the potency in inducing degeneration of cerebral 5-HT neurones. However since higher doses of MDEA (compared to MDMA) are probably necessary to induce mood changing effects, these data do not support any contention that this compound is a "safer" recreational drug than MDMA in terms of either acute toxicity or long term neurodegeneration.

摘要

给黑褐家鼠单次注射娱乐性使用的药物3,4-亚甲基二氧乙基苯丙胺(MDEA或“伊芙”)会导致急性剂量依赖性体温过高反应。腹腔注射35毫克/千克剂量的MDEA所产生的体温过高的峰值效应和持续时间,与腹腔注射15毫克/千克剂量的3,4-亚甲基二氧甲基苯丙胺(MDMA或“摇头丸”)相似。七天后,这个剂量的MDMA导致皮质、海马体和纹状体中5-羟色胺(5-HT)及其代谢物5-羟吲哚乙酸(5-HIAA)显著损失(约50%),并且皮质中[3H]-帕罗西汀结合也有类似损失:这些损失反映了MDMA诱导的5-HT神经末梢的神经毒性退化。相比之下,注射MDEA(15、25或35毫克/千克),即使是最高剂量,在皮质和海马体中也只产生了20%的损失,纹状体中没有减少。MDEA的神经毒性作用仅呈微弱的剂量依赖性。七天后,MDEA(35毫克/千克)和MDMA(15毫克/千克)都没有改变纹状体多巴胺含量。在诱导急性体温过高方面,MDEA的效力似乎约为MDMA的一半,在诱导大脑5-HT神经元退化方面,效力为MDMA的25%。然而,由于可能需要更高剂量的MDEA(与MDMA相比)才能产生情绪变化效应,这些数据并不支持任何关于该化合物在急性毒性或长期神经退化方面比MDMA“更安全”的娱乐性药物的论点。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验