Administration of aggregated beta-amyloid peptide (25-35) causes change in long-term potentiation in the hippocampus

A month after intracerebroventricular injection of aggregated beta-amyloid fragment 25-35 (7.5 nmol/ventricle), a significant change in in vivo long-term potentiation in hippocampus was demonstrated. The time course of the long-term potentiation was compared with that in sham-operated animals, a powerful and stable increase in the evoked potential amplitude was observed. This phenomenon can be related with the oxidative stress that was revealed in this model in our previous studies, and, as a consequence, with deterioration of ion homeostasis.