Disruption of hippocampal long-term potentiation by amyloid β
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The ability to obtain new memory is essential for our life quality and normal functioning. However, this process is disrupted in Alzheimer’s disease (AD). The consolidation of explicit memory, i.e. learning, is associated with plastic changes. The most important form of synaptic plasticity is long-term potentiation (LTP). In AD this process is disrupted by Amyloid β, a peptide that is also found in plaques. By the use of electrophysiological measurements the effect of Amyloid β derived diffusible ligands (ADDL) on basal synaptic transmission and LTP is studied in acute hippocampal slices of 4 month old male C57BL/6 mice. The Input-Output curve shows a significant decrease in fEPSP slope by high stimulus intensities in the ADDL treated group. Furthermore a significant lower fEPSP slope in percent of baseline is found after LTP induction in the ADDL treated slices. These results show that besides the disruption of LTP, there is also an impairment of basal synaptic transmission caused by ADDL.