Similar levels of long-term potentiation in amyloid precursor protein -null and wild-type mice in the CA1 region of picrotoxin treated slices.

Although mutations in amyloid precursor protein (APP) are known to be involved in the development of Alzheimer's disease in some individuals, the role of this protein in normal brain function is poorly understood. We have reported previously that in APP-null mice long-term potentiation (LTP) in the CA1 region of the hippocampus is present but its magnitude is reduced compared to wild-type littermate controls. In the present study, we have confirmed this deficit using a different theta burst induction protocol. Significantly, however, we find that this deficit is no longer apparent when LTP experiments are performed following blockade of gamma-aminobutyric acid(A) receptors. These results suggest that the LTP process per se is not altered by the absence of APP. The deficit may therefore be an indirect consequence of other changes in the hippocampus that occur in the APP-null animal.