Abstract
The role of intracellular amyloid β (iAβ) in Alzheimer's disease (AD) initiation and progression attracts more and more attention in recent years. To address whether iAβ induces early alterations of electrophysiological properties in cultured human primary neurons, we delivered iAβ with adeno-virus and measured the electrophysiological properties of infected neurons with whole-cell recordings. Our results show that iAβ induces an increase in neuronal resting membrane potentials, a decrease in K+ currents and a hyperpolarizing shift in voltage-dependent activation of K+ currents. These results suggest the electrophysiological impairments induced by iAβ may be responsible for its neuronal toxicity.
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