Objective: To explore the mechanism of beta-amyloid peptide (beta-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 beta-AP on transient outward potassium current were observed by a whole-cell recording patch clamp technique.
Results: beta-AP can significantly block transient potassium current in dose-dependent, time-dependent and partly voltage-dependent manners.
Conclusion: beta-AP may decrease the membrane conductance of K+ channels in hippocampal neurons, playing an important role in the pathophysiological mechanism of Alzheimer's disease.