Effects of beta-amyloid peptide on transient outward potassium current of acutely dissociated hippocampal neurons in CA1 sector in rats.
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.


CONCLUSIONS
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.
Xu
C
C
Department of Neurology, First Affiliated Hospital of Sun Yat-sen University of Medical Sciences, Guangzhou 510080, China.
Qian
C
C
Zhang
Z
Z
Wu
C
C
Zhou
P
P
Liang
X
X
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D006624:Hippocampus / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D018408:Patch-Clamp Techniques; D010446:Peptide Fragments / Q000494:pharmacology*; D015221:Potassium Channels / Q000187:drug effects* / Q000378:metabolism; D051381:Rats
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D015221:Potassium Channels; C074636:amyloid beta-protein (25-35)