Chu Chen
Neuroscience Center, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
Received 23 October 2005. Available online <span property="dc:creator" datatype="xsd:string">14 November 2005</span>.
Summary
Accumulation of the beta-amyloid peptide (Aß) is a primary event in the pathogenesis of Alzheimer's disease (AD). A transient A-type K + current has been shown to be affected by Aß (Good et al., 1996 [web page, PubMed record]). Here, I report that Aß (1–42) inhibits the dendritic A-type K + current in hippocampal CA1 pyramidal neurons, and this inhibition causes increases in back-propagating dendritic action potential amplitude and associated Ca 2+ influx.