Pharmacological alleviation of cholinergic lesion induced memory deficits in rats.
The cholinergic cells of the nucleus basalis of Meynert (nbM) have recently been found to degenerate in Alzheimer's disease and are thought to be at least partly responsible for the cognitive deficits which are characteristic of this disease. These experiments explored the behavioral effects of bilateral excitotoxic lesions of the nbM in adult rats. The first experiment showed that nbM lesions lead to a substantial deficit in the 24 hour retention of the habituation to a novel environment without affecting general exploratory behavior. The second experiment showed that this retention deficit is a general phenomenon reflected in the 72 hour retention of a one trial passive avoidance task. These retention deficits could be reversed by the postacquisition administration of the acetylcholinesterase inhibitor, physostigmine. These results support the hypothesis that central cholinergic systems are involved in the retention of learned responses, and suggest that cholinergic lesion induced retention deficits can be reversed by pharmacological means.
D000544:Alzheimer Disease / Q000503:physiopathology; D000818:Animals; D001479:Basal Ganglia / Q000502:physiology*; D002799:Cholinergic Fibers / Q000502:physiology*; D006801:Humans; D008297:Male; D008569:Memory Disorders / Q000188:drug therapy*; D009043:Motor Activity; D010830:Physostigmine / Q000627:therapeutic use; D051381:Rats; D011919:Rats, Inbred Strains; D013377:Substantia Innominata / Q000502:physiology*; D013997:Time Factors
D010830:Physostigmine