Butcher S P, Hamberger A, Morris R G
Department of Pharmacology, University of Edinburgh Medical School, UK.
Exp Brain Res. 1991;83(3):521-6. doi: 10.1007/BF00229829.
Chronic intraventricular infusion of the selective NMDA receptor antagonist AP5 appears to cause an impairment of spatial but not visual discrimination learning. However, Goddard (1986) has questioned whether this dissociation in task-selectivity reflects a difference in the underlying neural mechanisms or differential drug diffusion. Two experiments conducted to address this issue established (a) that chronic intraventricular infusion of AP5, at a dose sufficient to cause a spatial learning impairment, results in a relatively uniform distribution of the drug across the brain, and (b) that chronic bilateral intracortical infusion at sites very close to visual cortex also fails to impair visual discrimination learning. These findings argue against differential diffusion being a major cause of the sensitivity of spatial but not visual discrimination tasks to AP5, and raises the possibility that representational and procedural memory tasks may depend upon distinct cell-biological mechanisms of plasticity.
慢性脑室内注入选择性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂AP5似乎会导致空间辨别学习能力受损，但不会影响视觉辨别学习。然而，戈达德（1986年）质疑这种任务选择性的分离是否反映了潜在神经机制的差异或药物扩散的差异。为解决这个问题进行的两项实验表明：（a）以足以导致空间学习受损的剂量进行慢性脑室内注入AP5，会使药物在大脑中相对均匀地分布；（b）在非常靠近视觉皮层的部位进行慢性双侧皮层内注入，也不会损害视觉辨别学习。这些发现反对差异扩散是空间辨别任务而非视觉辨别任务对AP5敏感的主要原因，并提出了表象记忆和程序记忆任务可能依赖于不同的细胞生物学可塑性机制的可能性。
