Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4350420 | Neuroscience Letters | 2006 | 4 Pages |
Abstract
Amyloid-β (Aβ) is causally implicated in Alzheimer's disease and neuroplasticity failure has acquired validity as a possible mechanism of early AD pathogenesis. We have previously demonstrated that oligomeric Aβ 1-42 inhibits LTP in the dentate gyrus of rat hippocampal slices. We now show, using whole cell recordings in hippocampal granule cells, that oligomeric Aβ1-42 decreases neuronal excitability. In particular, Aβ1-42 application was associated with a decrease in the number of action potentials fired in response to current injection, and with an increase in the amplitude of the afterhyperpolarization. Reduced excitability may underlie the Aβ-mediated impairment in neuroplasticity, and ultimately may contribute to the memory loss in Alzheimer disease.
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Authors
Sung Hwan Yun, Georgi Gamkrelidze, W. Blaine Stine, Patrick M. Sullivan, Joseph F. Pasternak, Mary Jo LaDu, Barbara L. Trommer,