Linked Life Data

16470685

Source:http://linkedlifedata.com/resource/pubmed/id/16470685

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-3-23
pubmed:abstractText
Accumulation of amyloid (Abeta) peptides has been suggested to be the primary event in Alzheimer's disease. In neurons, K+ channels regulate a number of processes, including setting the resting potential, keeping action potentials short, timing interspike intervals, synaptic plasticity, and cell death. In particular, A-type K+ channels have been implicated in the onset of LTP in mammalian neurons, which is thought to underlie learning and memory. A number of studies have shown that Abeta peptides alter the properties of K+ currents in mammalian neurons. We set out to determine the effects of Abeta peptides on the neuronal A-type K+ channels of Drosophila. Treatment of cells for 18 h with 1 microM Abeta1-42 altered the kinetics of the A-type K+ current, shifting steady-state inactivation to more depolarized potentials and increasing the rate of recovery from inactivation. It also caused a decrease in neuronal viability. Thus it seems that alteration in the properties of the A-type K+ current is a prelude to the amyloid-induced death of neurons. This alteration in the properties of the A-type K+ current may provide a basis for the early memory impairment that was observed prior to neurodegeneration in a recent study of a transgenic Drosophila melanogaster line over-expressing the human Abeta1-42 peptide.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-3034
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
476-87
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Effects of amyloid peptides on A-type K+ currents of Drosophila larval cholinergic neurons.
pubmed:affiliation
Department of Human Anatomy and Genetics, MRC Functional Genetics Unit, University of Oxford, South Parks Road, Oxford OX1 3QX, United Kingdom. jackie.kidd@physiol.ox.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't