Impairments of long-term potentiation in hippocampal slices of beta-amyloid-infused rats

In this study, we investigated the neuronal activity of hippocampal slices from the beta-amyloid protein-infused (300 pmol/day for 10-11 days) rats us ing the extracellular recording technique. Perfusion of nicotine (50 mu M) reduced the amplitude of electrically evoked population spikes in the CA1 p yramidal cells of the vehicle control rats, but not in those of the beta-am yloid protein-infused rats, suggesting the impairment of nicotinic signalin g in the beta-amyloid protein-infused rats. Long-term potentiation induced by tetanic stimulations in CA1 pyramidal cells, which was readily observed in the vehicle control rats, was also impaired in the beta-amyloid protein- infused rats. Nicotinic blockade by adding hexamethonium into the perfused solution inhibited long-term potentiation induction. Taken together, our pr evious and present results suggest that beta-amyloid protein infusion impai rs the signal transduction mechanisms via nicotinic acetylcholine receptors . This dysfunction may be responsible, at least in part, for the impairment of long-term potentiation induction and may lead to learning deficits. (C) 1999 Elsevier Science B.V. All rights reserved.