Journal
NEUROBIOLOGY OF AGING
Volume 33, Issue 8, Pages 1609-1623Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2011.05.001
Keywords
Alzheimer's disease; Hippocampus; Pyramidal neuron; Intracellular calcium; Abeta; Beta-amyloid; Dendrite; Potassium channel
Categories
Funding
- Alzheimer's Association [NIRG-06-25509]
- National Institute on Aging [5R21AG029282-02]
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Amyloid-beta protein (A beta) is thought to play a central pathogenic role in Alzheimer's disease. A beta can impair synaptic transmission, but little is known about the effects of A beta on intrinsic cellular properties. Here we compared the cellular properties of CA1 hippocampal pyramidal neurons in acute slices from preplaque transgenic (Tg+) CRND8 mice and wild-type (Tg-) littermates. CA1 pyramidal neurons from Tg+ mice had narrower action potentials with faster decays than neurons from Tg- littermates. Action potential-evoked intracellular Ca2+ transients in the apical dendrite were smaller in Tg+ than in Tg- neurons. Resting calcium concentration was higher in Tg+ than in Tg- neurons. The difference in action potential waveform was eliminated by low concentrations of tetraethylammonium ions and of 4-aminopyridine, implicating a fast delayed-rectifier potassium current. Consistent with this suggestion, there was a small increase in immunoreactivity for Kv3.1b in stratum radiatum in Tg+ mice. These changes in intrinsic properties may affect information flow through the hippocampus and contribute to the behavioral deficits observed in mouse models and patients with early-stage Alzheimer's disease. (C) 2012 Elsevier Inc. All rights reserved.
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