AN AMYLOID BETA-PROTEIN FRAGMENT, A-BETA[12-28], EQUIPOTENTLY IMPAIRSPOST-TRAINING MEMORY PROCESSING WHEN INJECTED INTO DIFFERENT LIMBIC SYSTEM STRUCTURES
Jf. Flood et al., AN AMYLOID BETA-PROTEIN FRAGMENT, A-BETA[12-28], EQUIPOTENTLY IMPAIRSPOST-TRAINING MEMORY PROCESSING WHEN INJECTED INTO DIFFERENT LIMBIC SYSTEM STRUCTURES, Brain research, 663(2), 1994, pp. 271-276
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.