C Xu1, C Qian, Z Zhang, C Wu, P Zhou, X Liang. 1. Department of Neurology, First Affiliated Hospital of Sun Yat-sen University of Medical Sciences, Guangzhou 510080, China.
Abstract
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.
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.
Authors: Thomas M Morse; Nicholas T Carnevale; Pradeep G Mutalik; Michele Migliore; Gordon M Shepherd Journal: Front Neural Circuits Date: 2010-05-31 Impact factor: 3.492