Oxidative Stress Alters Physiological and Morphological Neuronal Properties

摘要

We investigated the effects of H2O2-induced oxidative stress on the delayed-rectifier current (IKDR), neuronal physiological and morphological properties. Measurements were obtained from hippocampal CA1 neurons in control solution and from the same neurons after exposure to oxidative stress (short- and long-term H2O2 external applications at 0.1, 1, and 10 mM). With short-term (6 min) H2O2 (1 mM) treatment, IKDR measured in the H2O2-containing solution (778 ± 23 pA, n = 20), was smaller than that measured in the control Ca2+-free Hepes solution (1,112 ± 38 pA, n = 20). Coenzyme Q10 (0.1 mM) pretreatment prevented the H2O2-induced inhibition of IKDR. With long-term (40, 80 min) H2O2 (0.1, 10 mM) treatment, the neuron lost its distinctive shape (rounded up) and the neurite almost disappeared. These results suggest that oxidative stress, which inhibits IKDR, can alter neural activity. The morphological changes caused by H2O2 support the idea that oxidative stress causes intracellular damage and compromises neural function.