Ischemia-induced object-recognition deficits in rats are attenuated by hippocampal ablation before or soon after ischemia.
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.
Mumby
D G
DG
Department of Psychology, University of British Columbia, Vancouver, Canada. mumby@vax2.concordia.ca
Wood
E R
ER
Duva
C A
CA
Kornecook
T J
TJ
Pinel
J P
JP
Phillips
A G
AG
D000818:Animals; D001070:Appetitive Behavior / Q000502:physiology; D001925:Brain Damage, Chronic / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology*; D001931:Brain Mapping; D002452:Cell Count; D015687:Cell Hypoxia / Q000502:physiology; D004193:Discrimination Learning / Q000502:physiology; D006624:Hippocampus / Q000098:blood supply / Q000503:physiopathology*; D008297:Male; D011939:Mental Recall / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D010364:Pattern Recognition, Visual / Q000502:physiology*; D016548:Prosencephalon / Q000098:blood supply / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012153:Retention, Psychology / Q000502:physiology