The effect of beta-amyloid-(1-40) was investigated on long-term potentiation of glutamatergic excitatory postsynaptic field potentials recorded in the inner molecular layer in the rat dentate gyrus in vitro. In the presence of 200 nM beta-amyloid-(1-40) there was an increase in long-term potentiation of 51%. Basal synaptic transmission was not affected. These results provide direct evidence that a relatively low concentration of beta-amyloid-(1-40) increases synaptic plasticity.