Butelman E R
Department of Psychology, University College London, UK.
Pharmacol Biochem Behav. 1990 Mar;35(3):533-6. doi: 10.1016/0091-3057(90)90285-p.
N-Methyl-d-aspartate (NMDA) receptors mediate the triggering of hippocampal long-term potentiation (LTP), a current physiological model of memory. This model was tested in the rat through the effect of (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801, a novel noncompetitive NMDA antagonist) on the radial arm maze (RAM) task with a 15-minute delay interposed at the midpoint choice. In two separate experiments, substereotypical drug doses of MK-801 and phencyclidine (a dissociative anesthetic with NMDA antagonist properties) were given intraperitoneally, before the trial or at the start of the delay. "Efficiency" was impaired in both tasks, but near-instantaneous use of encoded information seemed to be unaffected. This evidence would support a proposed role for NMDA-mediated pathways (and possibly LTP) in delayed stages of memory formation or use.
N-甲基-D-天冬氨酸(NMDA)受体介导海马体长期增强作用(LTP)的触发,LTP是当前记忆的生理模型。通过(+)-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺马来酸盐(MK-801,一种新型非竞争性NMDA拮抗剂)对放射状臂迷宫(RAM)任务的影响,在大鼠身上对该模型进行了测试,在中点选择时插入15分钟的延迟。在两个独立的实验中,在试验前或延迟开始时腹腔注射亚刻板剂量的MK-801和苯环己哌啶(一种具有NMDA拮抗剂特性的解离麻醉剂)。两项任务中的“效率”均受损,但编码信息的近乎即时使用似乎未受影响。这一证据将支持NMDA介导的通路(可能还有LTP)在记忆形成或使用的延迟阶段所起的作用。