Marek G J, Vosmer G, Seiden L S
Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637.
Brain Res. 1990 Apr 16;513(2):274-9. doi: 10.1016/0006-8993(90)90467-p.
A single large dose (100 mg/kg, s.c.) of methamphetamine (MA) is known to exert neurotoxic effects on dopaminergic neurons. The potency at which a series of dopamine (DA) uptake inhibitors blocked MA-induced neostriatal depletions (amfonelic acid (AFA) much greater than mazindol (MAZ) greater than or equal to bupropion (BUP) greater than benztropine (BENZ)) was similar to their potency at blocking 6-hydroxydopamine (6-OHDA) neurotoxicity in rats. Amfonelic acid was able to block long-term neostriatal DA depletions when given 8 h, but not 16 h, after a single large MA dose. These results suggest that an intact and functional DA uptake site is necessary for the development of MA-induced long-term DA depletions.
已知单次大剂量（100毫克/千克，皮下注射）的甲基苯丙胺（MA）会对多巴胺能神经元产生神经毒性作用。一系列多巴胺（DA）摄取抑制剂阻断MA诱导的新纹状体多巴胺耗竭的效力（氨苯利酸（AFA）远大于马吲哚（MAZ）大于或等于安非他酮（BUP）大于苯海索（BENZ））与其在阻断大鼠6-羟基多巴胺（6-OHDA）神经毒性方面的效力相似。在单次大剂量MA给药后8小时而非16小时给予氨苯利酸，能够阻断新纹状体长期的DA耗竭。这些结果表明，完整且功能正常的DA摄取位点对于MA诱导的长期DA耗竭的发生是必要的。
