Maj J, Rogóz Z, Skuza G
Institute of Pharmacology, Polish Academy of Sciences, Kraków.
J Neural Transm Gen Sect. 1991;85(3):169-79. doi: 10.1007/BF01244943.
MK-801, a non-competitive NMDA receptor antagonist, induced the locomotor hyperactivity in rats. Imipramine (IMI), amitriptyline (AMI), citalopram (CIT) given acutely increased the MK-801-induced locomotor hyperactivity. Mianserin (MIA) showed a similar but weaker effect. Haloperidol completely blocked the hyperactivity induced by the antidepressant drug (AD) + MK-801. Prazosin had an only weak antagonistic effect. Repeated treatment with AD increased the MK-801 locomotor hyperactivity to a greater extent than acute treatment. This effect was completely blocked by haloperidol and only partly by prazosin. The obtained results indicate that the dopamine system may be involved, at least in part, in the potentiating effect of the combined treatment with AD + MK-801.
MK-801是一种非竞争性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂,可诱发大鼠运动活动亢进。急性给予丙咪嗪(IMI)、阿米替林(AMI)、西酞普兰(CIT)可增强MK-801诱发的运动活动亢进。米安色林(MIA)显示出类似但较弱的作用。氟哌啶醇完全阻断了抗抑郁药(AD)+MK-801诱发的活动亢进。哌唑嗪仅有微弱的拮抗作用。与急性给药相比,重复给予AD能更大程度地增强MK-801诱发的运动活动亢进。这种作用被氟哌啶醇完全阻断,仅部分被哌唑嗪阻断。所得结果表明,多巴胺系统可能至少部分参与了AD+MK-801联合治疗的增强作用。