RESUMEN
Fisher 344 rats underwent bilateral nucleus basalis magnocellularis (NBm) lesioning followed by testing in a delayed nonmatching-to-sample T-maze task. Both lesion and control animals acquired the task although the NBm animals were mildly impaired on acquisition and on trials to criterion. Increasing the delay reduced accuracy of performance equally in both groups. The NBm lesion did not alter the level of several thalamic amino acids. These data indicate that NBm lesioning does not produce a significant impairment in working or reference memory in this task and supports the hypothesis that NBm lesioning impairs attention.
Asunto(s)
Ganglios Basales/fisiología , Aprendizaje/fisiología , Tálamo/metabolismo , Aminoácidos/metabolismo , Animales , Corteza Cerebral/enzimología , Corteza Cerebral/metabolismo , Colina O-Acetiltransferasa/metabolismo , Ácido Iboténico/farmacología , Masculino , Memoria/fisiología , Memoria a Corto Plazo/fisiología , Neurotransmisores/metabolismo , Ratas , Ratas Endogámicas F344 , Ácido gamma-Aminobutírico/metabolismoRESUMEN
Rats received a unilateral lesion of the nucleus basalis by infusion of ibotenic acid. Two weeks after the lesion, osmotic minipumps were implanted, that infused 1 microgram human recombinant nerve growth factor (NGF) or cytochrome-C per day into the lateral ventricle. After four weeks of treatment, release of acetylcholine was measured in the frontal neocortex by means of in-vivo microdialysis. Release was decreased by 75% on the lesioned side; perfusion with 100 mM KCl increased release on the intact side by 130% and on the lesioned side by 80%. Treatment with NGF increased release on the lesioned side twofold, but had no effect on release on the intact side.