Hydrogen peroxide modulates K + ion currents in cultured Aplysia sensory neurons

Abstract

Hydrogen peroxide (H 2O 2) causes oxidative stress and is considered a mediator of cell death in various organisms. Our previous studies showed that prolonged (>6 h) treatment of Aplysia sensory neurons with 1 mM H 2O 2 produced hyperpolarization of the resting membrane potential, followed by apoptotic morphological changes. In this study, we examined the effect of H 2O 2 on the membrane conductance of Aplysia sensory neurons. Hyperpolarization was induced by 10 mM H 2O 2 within 1 h, and this was attributed to increased membrane conductance. In addition, treatment with 10 mM H 2O 2 for 3 min produced immediate depolarization, which was due to decreased membrane conductance. The H 2O 2-induced hyperpolarization and depolarization were completely blocked by dithiothreitol, a disulfide-reducing agent. The later increase of membrane conductance induced by H 2O 2 was completely blocked by 100 mM TEA, a K + channel blocker, suggesting that H 2O 2-induced hyperpolarization is due to the activation of K + conductance. However, the inhibition of K + efflux by TEA did not protect against H 2O 2-induced cell death in cultured Aplysia sensory neurons, which indicates that the signal pathway leading to H 2O 2-induced cell death is more complicated than expected.