Electrophysiological Functions of Intracellular Amyloid β in Specific for Cultured Human Neurones and its Impairment Properties

Abstract

Prevailing role of intracellular amyloid <TEX>${\beta}$</TEX> (<TEX>$iA{\beta}$</TEX>) in Alzheimer's disease (AD) initiation and progression attracts more and more attention in recent years. To address whether <TEX>$iA{\beta}$</TEX> induces early alterations of electrophysiological properties in cultured human primary neurons, we delivered <TEX>$iA{\beta}$</TEX> with adenovirus and measured the electrophysiological properties of infected neurons with whole-cell recordings. Our results show that <TEX>$iA{\beta}$</TEX> induces an increase in neuronal resting membrane potentials, a decrease in <TEX>$K^+$</TEX> currents and a hyperpolarizing shift in voltage-dependent activation of <TEX>$K^+$</TEX> currents. These results suggest the electrophysiological impairments induced by <TEX>$iA{\beta}$</TEX> may be responsible for its neuronal toxicity.