Abstract
Alcohol-induced memory impairment in man has been attributed to deficiencies in subcortical noradrenergic1 and cholinergic2,3 systems, as well as to damage in midbrain structures4. Korsakoff's psychosis, a disease in which alcohol poisoning causes apparently irreversible memory defects, is characterized by lesions in cholinergic5 and noradrenergic6 nuclei and by a decrease in the activity of choline acetyltransferase7–10 (ChAT) and the content of noradrenaline7 (NA) in forebrain areas such as cerebral cortex and hippocampus, innervated by these nuclei11,12. Prolonged intake of ethanol in rodents similarly produces signs of noradrenergic 1,13–15 and cholinergic16,17 deafferentation in the cortex and hippocampus, as well as persistent memory deficits17–19. To test whether alcohol-induced memory impairments depend on cholinergic deafferentation, we transplanted cholinergic-rich fetal basal forebrain cell suspensions20 into the cortex and hippocampus of alcohol-treated rats. The substantial and persistent memory losses produced in our rats by ethanol intake were associated with an impairment of cholinergic function, and were reversed by cholinergic-rich transplants into cortex and hippocampus.
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Arendt, T., Allen, Y., Sinden, J. et al. Cholinergic-rich brain transplants reverse alcohol-induced memory deficits. Nature 332, 448–450 (1988). https://doi.org/10.1038/332448a0
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DOI: https://doi.org/10.1038/332448a0
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