Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
- 14 July 2010
- journal article
- video audio-media
- Published by MyJove Corporation in Journal of Visualized Experiments
- No. 41,p. e1884
- https://doi.org/10.3791/1884
Abstract
Impairment of synaptic connections is likely to underlie the subtle amnesic changes occurring at the early stages of Alzheimer s Disease (AD). beta-amyloid (A beta), a peptide produced in high amounts in AD, is known to reduce Long-Term Potentiation (LTP), a cellular correlate of learning and memory. Indeed, LTP impairment caused by A beta is a useful experimental paradigm for studying synaptic dysfunctions in AD models and for screening drugs capable of mitigating or reverting such synaptic impairments. Studies have shown that A beta produces the LTP disruption preferentially via its oligomeric form. Here we provide a detailed protocol for impairing LTP by perfusion of oligomerized synthetic A beta1-42 peptide onto acute hippocampal slices. In this video, we outline a step-by-step procedure for the preparation of oligomeric A beta(1-42;). Then, we follow an individual experiment in which LTP is reduced in hippocampal slices exposed to oligomerized A beta(1-42;) compared to slices in a control experiment where no A beta(1-42;) exposure had occurred.Keywords
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