Mumby D G, Wood E R, Duva C A, Kornecook T J, Pinel J P, Phillips A G
Department of Psychology, University of British Columbia, Vancouver, Canada.
Behav Neurosci. 1996 Apr;110(2):266-81. doi: 10.1037//0735-7044.110.2.266.
The literature on the role of the hippocampus in object-recognition contains a paradox: Transient forebrain ischemia (ISC) produces hippocampal damage and severe deficits on the delayed nonmatching-to-sample (DNMS) task, yet hippocampal ablation (ABL) produces milder deficits. Experiment 1 confirmed that pretrained rats display severe DNMS deficits following ISC, but not ABL. Ischemia produced loss of CA1 neurons, but no obvious extrahippocampal damage. In Experiments 2 and 3, ISC rats from Experiment 1 received ABL, and ABL rats received ISC; neither treatment affected DNMS performance. In Experiment 4, rats that received ISC followed 1 hr later by ABL displayed only mild deficits. It is hypothesized that ISC-induced DNMS deficits are due to extrahippocampal damage produced by pathogenic processes that involve the hippocampus.
短暂性前脑缺血（ISC）会导致海马体损伤以及在延迟非匹配样本（DNMS）任务中出现严重缺陷，但海马体切除（ABL）产生的缺陷则较轻。实验1证实，经过预训练的大鼠在经历ISC后会出现严重的DNMS缺陷，但ABL后则不会。缺血导致CA1神经元丧失，但没有明显的海马体外损伤。在实验2和3中，实验1中的ISC大鼠接受了ABL，而ABL大鼠接受了ISC；两种处理均未影响DNMS表现。在实验4中，先接受ISC 1小时后再接受ABL的大鼠仅表现出轻微缺陷。据推测，ISC诱导的DNMS缺陷是由于涉及海马体的致病过程产生的海马体外损伤所致。
