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Beta-amyloid peptide induces the expression of voltage dependent outward rectifying K+ channels in rat microglia.

Authors
Chung, S; Lee, J; Joe, EH; Uhm, DY
Citation
Neuroscience letters, 300(2):67-70, 2007
Journal Title
Neuroscience letters
ISSN
0304-39401872-7972
Abstract
Upregulation of voltage-dependent outward rectifying K+ (Kv) channels has been reported in activated microglia. Since beta-amyloid peptide (A beta) is known to activate microglia, we tested whether the exposure of cultured rat microglia to A beta fragment 25-35 (A beta 25-35) induced the Kv current. A beta 25-35 in 5-200 nM concentration range significantly increased Kv current density, while there was small change in inward rectifying K+ current density. The full length A beta peptide (A beta 1-42) also increased Kv current. However, the control peptide, A beta 35-25, did not induce Kv current. Most of the Kv current induced by A beta was specifically blocked by the presence of antisense deoxyoligonucleotides against Kv1.3, and Kv1.5. Thus, it is concluded that we have identified Kv1.3 and Kv1.5 as the channel types expressed in A beta-treated microglia.
MeSH terms
Alzheimer Disease/metabolismAlzheimer Disease/physiopathologyAmyloid beta-Peptides/metabolismAmyloid beta-Peptides/pharmacology*AnimalsAnimals, NewbornCells, Cultured/drug effectsCells, Cultured/metabolismGene Expression/drug effects*Gene Expression/physiologyKv1.3 Potassium ChannelKv1.5 Potassium ChannelMembrane Potentials/drug effects*Membrane Potentials/physiologyMicroglia/drug effects*Microglia/metabolismNerve Degeneration/metabolismNerve Degeneration/physiopathologyOligodeoxyribonucleotides, Antisense/pharmacologyPatch-Clamp TechniquesPeptide Fragments/pharmacologyPotassium Channels/drug effects*Potassium Channels/geneticsPotassium Channels/metabolismPotassium Channels, Voltage-Gated*RatsRats, Sprague-Dawley
PMID
11207376
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
조, 은혜
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