Walker D L, Gold P E
Neuroscience Graduate Program, University of Virginia, Charlottesville 22903.
Behav Neural Biol. 1992 Jul;58(1):69-71. doi: 10.1016/0163-1047(92)90952-z.
N-Methyl-D-aspartate (NMDA) receptor antagonists disrupt learning on a variety of tasks. Previous findings indicate that glucose, naloxone, and physostigmine ameliorate learning deficits produced by several treatments. The present experiment examines whether these agents also reverse the amnestic effects of NMDA receptor blockade. Mice were tested for spontaneous alternation performance in a Y-maze. The animals received either saline or the NMDA antagonist, NPC 12626 (35 mg/kg, IP), 50 min prior to testing and received an additional injection of saline, glucose, naloxone, or physostigmine 30 min prior to testing. NPC 12626 significantly decreased alternation scores. Glucose (250 mg/kg), physostigmine (0.01 mg/kg), and naloxone (1 mg/kg) reversed the effects of NPC 12626. Thus, impairments of learning after NMDA receptor blockade share with other amnestic conditions the susceptibility to attenuation by glucose, naloxone, and physostigmine.
N-甲基-D-天冬氨酸（NMDA）受体拮抗剂会干扰多种任务的学习。先前的研究结果表明，葡萄糖、纳洛酮和毒扁豆碱能改善几种处理所产生的学习缺陷。本实验旨在研究这些药物是否也能逆转NMDA受体阻断所产生的遗忘效应。在Y型迷宫中对小鼠进行自发交替行为测试。在测试前50分钟，动物接受生理盐水或NMDA拮抗剂NPC 12626（35毫克/千克，腹腔注射），并在测试前30分钟额外注射生理盐水、葡萄糖、纳洛酮或毒扁豆碱。NPC 12626显著降低了交替得分。葡萄糖（250毫克/千克）、毒扁豆碱（0.01毫克/千克）和纳洛酮（1毫克/千克）逆转了NPC 12626的作用。因此，NMDA受体阻断后的学习障碍与其他遗忘症情况一样，对葡萄糖、纳洛酮和毒扁豆碱的减弱作用敏感。
