Comparative effects of cholinergic drugs and lesions of nucleus basalis or fimbria-fornix on delayed matching in rats.

Article date: 1985/1/1

PubMed ID: 1161993

Journal name: Psychopharmacology (ISSN: 0033-3158)


To provide a more specific test of memory impairments following lesions to central cholinergic systems, rats were trained on an operant delayed matching task. Ibotenic acid lesions of the nucleus basalis produced a disruption of performance at all delay intervals (a parallel downward shift in the delay-performance curve). By contrast, fimbria-fornix transections had no effects at short delays, but produced a progressively greater impairment as the delays lengthened (an increased downward slope of the delay-performance curve). Scopolamine produced a dose-dependent disruption of performance, apparent at the shortest delays but greater at longer delays, that was similar to the two lesion deficits combined, whereas physostigmine induced a mild but significant enhancement of performance. The results support the hypothesis that disruption of hippocampal circuitries, including cholinergic afferents via the fimbria-fornix, produces short-term or working memory impairments, whereas disruption of the cortical cholinergic system implicates more stable long-term aspects of task performance. Peripherally administered cholinergic drugs produce both types of effect and thus may influence both systems.

Author List: Dunnett S B

Publication Types: Journal Article

Substances mentioned in the article: Methamphetamine; Scopolamine Hydrobromide; Physostigmine;

Mesh terms: Animals; Basal Ganglia/physiology; Brain Mapping; Cerebral Cortex/physiology; Cholinergic Fibers/physiology; Female; Hippocampus/physiology; Memory/physiology; Methamphetamine/pharmacology; Neural Pathways/physiology; Physostigmine/pharmacology; Rats; Rats, Inbred Strains; Scopolamine Hydrobromide/pharmacology; Septum Pellucidum/physiology; Substantia Innominata/physiology;

Citations: - Cholinergic ventral forebrain grafts into the neocortex improve passive avoidance memory in a rat model of Alzheimer disease.

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