Amyloid-beta1-42 Reduces Neuronal Excitability in Mouse Dentate Gyrus.
From: Department of Pediatrics and Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60614, USA.
Neuroscience letters
- Publish Date: Jul 2006
- ISSN: 0304-3940
- Volume: 403
- Issue: 1-2
- Pages: 162-5
- Medium: Print
- Language: English
- Citation (JAMA): Yun Sung Hwan, Gamkrelidze Georgi, Stine W Blaine, et al. Amyloid-beta1-42 Reduces Neuronal Excitability in Mouse Dentate Gyrus.. Neurosci. Lett. Jul 2006;403:162-5
Abstract
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.
Mesh Headings (Keywords): Action Potentials, Amyloid beta-Protein, Animals, Biopolymers, Dentate Gyrus, Long-Term Potentiation, Male, Mice, Mice, Inbred C57BL, Neurons, Patch-Clamp Techniques, Peptide Fragments
Check for Full Text / PubMed Unique Identifier (PMID): 16765515
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