RESUMEN
Ischemia-induced cell loss in the CA1 region of the dorsal hippocampus results in severe deficits on delayed non-matching-to-sample (DNMS), whereas hippocampectomy produces little or no impairment, suggesting that partial hippocampal damage is more detrimental to DNMS performance than total ablation. To test this hypothesis, rats with or without preoperative DNMS training were given partial cytotoxic lesions of the dorsal hippocampus. When tested, neither group displayed any DNMS deficits despite widespread cell loss in the CA1 and other regions of the dorsal hippocampus. In the final experiments, rats tested previously on DNMS were found to be impaired on the Morris water maze. The finding that partial hippocampal lesions disrupt spatial memory while leaving object-recognition memory intact indicates a specialized role for the hippocampus in mnemonic processes.
Asunto(s)
Amnesia/fisiopatología , Lesiones Encefálicas/fisiopatología , Aprendizaje Discriminativo/efectos de los fármacos , Hipocampo/efectos de los fármacos , Aprendizaje por Laberinto/efectos de los fármacos , Reconocimiento Visual de Modelos/efectos de los fármacos , Lóbulo Temporal/fisiopatología , Animales , Corteza Cerebral/lesiones , Corteza Cerebral/patología , Aprendizaje Discriminativo/fisiología , Modelos Animales de Enfermedad , Agonistas de Aminoácidos Excitadores , Hipocampo/lesiones , Hipocampo/patología , Hipocampo/fisiopatología , Masculino , Aprendizaje por Laberinto/fisiología , Memoria/efectos de los fármacos , Memoria/fisiología , N-Metilaspartato , Orientación/efectos de los fármacos , Orientación/fisiología , Reconocimiento Visual de Modelos/fisiología , Ratas , Ratas Wistar , Factores de TiempoRESUMEN
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.