K+ channel openers protect hippocampal neurons against oxidative injury and amyloid β-peptide toxicity

Yadong Goodman, Mark P. Mattson

Research output: Contribution to journalArticle

Abstract

Potassium channel openers (KCOs) such as diazoxide and levochromakalim can protect cardiac myocytes against ischemic injury and neurons against excitotoxic injury, presumably because of their ability to hyperpolarize the plasma membrane and reduce calcium influx. We now report that diazoxide, levocromakalim (LCC), and to a lesser extent pinacidil, protect cultured rat hippocampal neurons against oxidative injury induced by exposure to FeSO4 and amyloid β-peptide (Aβ). Imaging studies of intracellular peroxide levels revealed that KCOs suppressed the generation of peroxides induced by FeSO4 and Aβ. KCOs were effective in protecting neurons against oxidative insults in the presence of the K+ channel blockers glibenclamide and 4-aminopyridine indicating that their protective mechanism involved actions in addition to activation of K+ channels. The data suggest that KCOs may be of therapeutic value in an array of neurodegenerative disorders that involve oxidative injury.

Original languageEnglish (US)
Pages (from-to)328-332
Number of pages5
JournalBrain Research
Volume706
Issue number2
DOIs
StatePublished - Jan 15 1996
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Diazoxide
  • Dichlorofluorescin
  • Hydrogen peroxide
  • Levochromakalim
  • Pinacidil

ASJC Scopus subject areas

  • Neuroscience(all)

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