Amyloid-beta1-42 reduces neuronal excitability in mouse dentate gyrus.

Journal Article (Journal Article)

Amyloid-beta (Abeta) 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 Abeta(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 Abeta(1-42) decreases neuronal excitability. In particular, Abeta(1-42) 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 Abeta-mediated impairment in neuroplasticity, and ultimately may contribute to the memory loss in Alzheimer disease.

Full Text

Duke Authors

Cited Authors

  • Yun, SH; Gamkrelidze, G; Stine, WB; Sullivan, PM; Pasternak, JF; Ladu, MJ; Trommer, BL

Published Date

  • July 31, 2006

Published In

Volume / Issue

  • 403 / 1-2

Start / End Page

  • 162 - 165

PubMed ID

  • 16765515

Pubmed Central ID

  • PMC3752836

International Standard Serial Number (ISSN)

  • 0304-3940

Digital Object Identifier (DOI)

  • 10.1016/j.neulet.2006.04.065


  • eng

Conference Location

  • Ireland