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Updated: Jun 23, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
Published on: July 14, 2010
Alzheimer beta-amyloid blocks epileptiform activity in hippocampal neurons
Fernando J Sepúlveda1, Carlos Opazo, Luis G Aguayo
1Laboratory of Neurophysiology, Department of Physiology, University of Concepción, Chile.
Abstract:
Several studies showed that hippocampal neurons respond with an increase in synaptic transmission after chronic blockade of GABA(A) receptors with bicuculline, a neuroplastic phenomenon likely associated to epileptiform states. Here, we tested the effect of Abeta(1-40) oligomers/aggregates, believed to be involved in Alzheimer's Disease (AD) genesis, on this type of synaptic plasticity. In the presence of bicuculline, the frequency of miniature currents increased from 1.2+/-0.4 Hz to 3.1+/-0.6 Hz (n=6, p<0.05). Similarly, current amplitude increased from 45+/-3 pA to 81+/-11 pA (n=5, p<0.05). These effects were completely inhibited in the presence of Abeta(1-40) aggregates. Data suggest that Abeta aggregates exert their influence principally by blocking synaptic transmission and altering the transcriptional pathway associated with CREB-p. In conclusion, neurons exposed to aggregated Abeta(1-40) showed a reduced level of neuronal plasticity and this suggests that they might be acting as anti-epileptiform modulators.
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