Using in vivo microdialysis techniques, the effects of RTI-55 and/or cocaine on extracellular dopamine (DA) concentrations were measured in the nucleus accumbens (NACC) of freely moving rats. In control animals, cocaine (20 mg/kg) increased NACC DA approximately 458% 60 minutes following administration, returning to baseline values within 200 minutes. Similarly, RTI-55 administration (0.25 mg/kg) increased NACC DA levels approximately 347%. When combined, however, cocaine further increased NACC DA to 705% of baseline values when given 4 hours following RTI-55. This increase was significantly larger than cocaine alone (P < 0.05). In addition, chronic RTI-55 administration (5 days) further potentiated cocaine's ability to increase NACC DA (783%) but this did not reach statistical significance (P > 0.1) compared to acute RTI55/cocaine animals. These findings indicate that RTI-55, a drug that binds directly to the dopamine transporter (DAT) with higher affinity than cocaine, does not appear to be effective in attenuating cocaine's effects on NACC dopamine levels. In fact, acute RTI-55 potentiates cocaine's effects on NACC DA.

译文

使用体内微透析技术,在自由运动的大鼠伏隔核 (NACC) 中测量了RTI-55和/或可卡因对细胞外多巴胺 (DA) 浓度的影响。在对照动物中,可卡因 (20 mg/kg) 在给药后约60分钟458% 增加NACC DA,在200分钟内恢复到基线值。类似地,RTI-55施用 (0.25 mg/kg) 使NACC DA水平增加约347%。然而,当合并时,当RTI-55后4小时给予时,可卡因进一步增加NACC DA至基线值的705%。这一增加显著大于单独使用可卡因 (P <0.05)。此外,慢性RTI-55给药 (5天) 进一步增强了可卡因增加NACC DA (783%) 的能力,但与急性RTI55/可卡因动物相比,这没有达到统计学意义 (P> 0.1)。这些发现表明,RTI-55是一种直接与多巴胺转运蛋白 (DAT) 结合的药物,其亲和力高于可卡因,似乎无法有效减轻可卡因对NACC多巴胺水平的影响。实际上,急性RTI-55增强了可卡因对NACC DA的影响。

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