Amyloid-beta1-42 reduces neuronal excitability in mouse dentate gyrus.
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.
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Related Subject Headings
- Peptide Fragments
- Patch-Clamp Techniques
- Neurons
- Mice, Inbred C57BL
- Mice
- Male
- Long-Term Potentiation
- In Vitro Techniques
- Dentate Gyrus
- Biopolymers
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Peptide Fragments
- Patch-Clamp Techniques
- Neurons
- Mice, Inbred C57BL
- Mice
- Male
- Long-Term Potentiation
- In Vitro Techniques
- Dentate Gyrus
- Biopolymers