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• W1529942406 abstract "Abstract Increased activity of plasma membrane K + channels, leading to decreased cytoplasmic K + concentrations, occurs during neuronal cell death. In the present study, we showed that the neurotoxic β‐amyloid peptide Aβ 25−35 caused a dose‐dependent (0.1–10 µ m ) and time‐dependent (> 12 h) enhancement of both inactivating and non‐inactivating components of voltage‐dependent K + (VGK) currents in nerve growth factor‐differentiated rat phaeochromocytoma (PC‐12) cells and primary rat hippocampal neurones. Similar effects were exerted by Aβ 1−42 , but not by the non‐neurotoxic Aβ 35−25 peptide. Aβ 25−35 and Aβ 1−42 caused an early (15–20 min) increase in intracellular Ca 2+ concentration. This led to an increased production of reactive oxygen species (ROS), which peaked at 3 h and lasted for 24 h; ROS production seemed to trigger the VGK current increase as vitamin E (50 µ m ) blocked both the Aβ 25−35 ‐ and Aβ 1−42 ‐induced ROS increase and VGK current enhancement. Inhibition of protein synthesis (cycloheximide, 1 µg/mL) and transcription (actinomycin D, 50 ng/mL) blocked Aβ 25−35 ‐induced VGK current enhancement, suggesting that this potentiation is mediated by transcriptional activation induced by ROS. Interestingly, the specific nuclear factor‐κB inhibitor SN‐50 (5 µ m ), but not its inactive analogue SN‐50M (5 µ m ), fully counteracted Aβ 1−42 ‐ or Aβ 25−35 ‐induced enhancement of VGK currents, providing evidence for a role of this family of transcription factors in regulating neuronal K + channel function during exposure to Aβ." @default.
• W1529942406 created "2016-06-24" @default.
• W1529942406 creator A5017571914 @default.
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• W1529942406 creator A5071813092 @default.
• W1529942406 date "2005-06-22" @default.
• W1529942406 modified "2023-10-16" @default.
• W1529942406 title "Nuclear factor-κB activation by reactive oxygen species mediates voltage-gated K+ current enhancement by neurotoxic β-amyloid peptides in nerve growth factor-differentiated PC-12 cells and hippocampal neurones" @default.
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• W1529942406 doi "https://doi.org/10.1111/j.1471-4159.2005.03075.x" @default.
• W1529942406 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15969743" @default.
• W1529942406 hasPublicationYear "2005" @default.
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