Uzbay I T, Wallis C J, Lal H, Forster M J
Department of Medical Pharmacology, Faculty of Medicine, Gülhane Military Medical Academy, Etlik, Ankara, Turkey.
Behav Brain Res. 2000 Feb;108(1):57-61. doi: 10.1016/s0166-4328(99)00129-1.
Effects of MK-801 and ketamine, N-methyl-D-aspartate (NMDA) receptor blockers, on cocaine-stimulated locomotor activity were investigated in male Swiss-Webster mice. MK-801 (0.25, 0.5, 1.0 and 2.5 mg/kg), ketamine (10, 25 and 50 mg/kg) or saline was injected 20 min before cocaine (5, 10 and 20 mg/kg i.p.). Locomotor activity was measured for 30 min immediately following cocaine treatment. All doses of the drugs were also tested for ability to depress or stimulate locomotor activity in the naive (no cocaine-treated) mice. Cocaine produced a dose-dependent increase in locomotor activity that was blocked dose-dependently by MK-801 or ketamine. The blockade by MK-801 was more prominent than by ketamine. Our results may suggest that cocaine-induced locomotor stimulation in mice is modulated via NMDA receptor mediated mechanisms.
在雄性瑞士韦伯斯特小鼠中研究了N-甲基-D-天冬氨酸（NMDA）受体阻滞剂MK-801和氯胺酮对可卡因刺激的运动活性的影响。在腹腔注射可卡因（5、10和20mg/kg）前20分钟，注射MK-801（0.25、0.5、1.0和2.5mg/kg）、氯胺酮（10、25和50mg/kg）或生理盐水。在可卡因处理后立即测量30分钟的运动活性。还测试了所有剂量的药物在未用可卡因处理的（未接触过可卡因的）小鼠中抑制或刺激运动活性的能力。可卡因产生了剂量依赖性的运动活性增加，而MK-801或氯胺酮以剂量依赖性方式阻断了这种增加。MK-801的阻断作用比氯胺酮更显著。我们的结果可能表明，可卡因诱导的小鼠运动刺激是通过NMDA受体介导的机制调节的。
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