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D1 拮抗剂与 D2 拮抗剂对(±)3,4-亚甲二氧基甲基苯丙胺和可卡因破坏延迟匹配样本任务表现的作用的衰减。

Attenuation of the disruptive effects of (+/-)3,4-methylenedioxymethamphetamine and cocaine on delayed matching-to-sample performance with D1 versus D2 antagonists.

机构信息

School of Psychology, Victoria University of Wellington, New Zealand.

出版信息

Addict Biol. 2013 Nov;18(6):912-20. doi: 10.1111/j.1369-1600.2011.00389.x. Epub 2011 Oct 13.

DOI:10.1111/j.1369-1600.2011.00389.x
PMID:21995578
Abstract

Evidence suggests that acute exposure to (+/-)3,4-methylenedioxymethamphetamine (MDMA) produces qualitatively similar effects on recognition task performance as other stimulant-type drugs. The current study examined whether there was a similar neurochemical basis to these memory effects by examining the effects of a D1 receptor antagonist (SCH23390) and D2 antagonist (eticlopride) on MDMA- or cocaine-induced impairments in delayed matching-to-sample performance in rats. At low doses it was shown that eticlopride was ineffective in antagonizing either MDMA or cocaine's effects, and at higher doses exacerbated their effects. In contrast, the D1 receptor antagonist SCH23390 was only able to significantly attenuate the disruption caused by MDMA, but not cocaine's effects. Therefore, although present evidence suggests that the effect of acute MDMA on memory-task performance may be related to its effects at D1 receptor sites, there may be differences between MDMA and cocaine in the precise neurochemical pathways involved despite their having similar cognitive effects.

摘要

有证据表明,急性暴露于(±)3,4-亚甲基二氧甲基苯丙胺(MDMA)会对识别任务的表现产生与其他兴奋剂类药物类似的影响。本研究通过检查 D1 受体拮抗剂(SCH23390)和 D2 拮抗剂(eticlopride)对 MDMA 或可卡因引起的大鼠延迟匹配样本表现损伤的影响,来探究这些记忆效应是否存在类似的神经化学基础。结果表明,在低剂量下,eticlopride 无法拮抗 MDMA 或可卡因的作用,而在高剂量下则加剧了它们的作用。相比之下,D1 受体拮抗剂 SCH23390 仅能显著减轻 MDMA 引起的干扰,但不能减轻可卡因的作用。因此,尽管目前的证据表明,急性 MDMA 对记忆任务表现的影响可能与其在 D1 受体部位的作用有关,但 MDMA 和可卡因在涉及的精确神经化学途径中可能存在差异,尽管它们具有相似的认知效应。

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