Objective To explore the mechanism of β-amyloid peptide (β-AP) in Alzheimer's disease at ionic channel level.Methods Hippocampal CA1 neurons of 7-21 days' rats were acutely dissociated and the effects of β-AP on transient outward potassium current were observed by a whole-cell recording patch clamp technique.Results β-AP can significantly block transient potassium current in dose-dependent, time-dependent and partly voltage-dependent manners.Conclusion β-AP may decrease the membrane conductance of K+ channels in hippocampal neurons, playing an important role in the pathophysiological mechanism of Alzheimer's disease.
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