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 language | English (US) |
---|---|
Pages (from-to) | 328-332 |
Number of pages | 5 |
Journal | Brain Research |
Volume | 706 |
Issue number | 2 |
DOIs | |
State | Published - Jan 15 1996 |
Externally published | Yes |
Keywords
- Alzheimer's disease
- Diazoxide
- Dichlorofluorescin
- Hydrogen peroxide
- Levochromakalim
- Pinacidil
ASJC Scopus subject areas
- General Neuroscience