AN AMYLOID BETA-PROTEIN FRAGMENT, A-BETA[12-28], EQUIPOTENTLY IMPAIRSPOST-TRAINING MEMORY PROCESSING WHEN INJECTED INTO DIFFERENT LIMBIC SYSTEM STRUCTURES

Previously, amyloid beta-protein (A beta) fragments 1-28, 12-28 and 12 -20 were found to impair retention in mice when injected intracerebrov entricularly after footshock active avoidance training. We now have me asured the dose-dependence of amnestic effects of peptide 12-28 stereo tactically injected into amygdala, caudate, hippocampus, mammillary bo dies and septum, which limbic structures are known to be involved in m emory processing and into the medial thalamus, which largely is involv ed in sensory processing during training. Peptide 12-28 impaired reten tion with remarkably similar efficacy when injected into limbic struct ures but was not at all amnestic upon thalamic injection. Present resu lts together with those in the literature lead us to suggest that A be ta may exert dysregulatory cognitive effects by incoordination of K+-c hannel function in neurons. glia and endothelial cells.