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J Neurophysiol 87: 2990-2995, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 6 June 2002, pp. 2990-2995
Copyright ©2002 by the American Physiological Society

Differential Oxidative Modulation of Voltage-Dependent K+ Currents in Rat Hippocampal Neurons

Wolfgang Müller and Katrin Bittner

Molekulare Zellphysiologie, Charité, Neurowissenschaftliches Forschungszentrum, D-10117 Berlin, Germany

Müller, Wolfgang and Katrin Bittner. Differential Oxidative Modulation of Voltage-Dependent K+ Currents in Rat Hippocampal Neurons. J. Neurophysiol. 87: 2990-2995, 2002. Oxidative stress is enhanced by [Ca2+]i-dependent stimulation of phospholipases and mitochondria and has been implicated in immune defense, ischemia, and excitotoxicity. Using whole cell recording from hippocampal neurons, we show that arachidonic acid (AA) and hydrogen peroxide (H2O2) both reduce the transient K+ current IA by -54 and -68%, respectively, and shift steady-state inactivation by -10 and -15 mV, respectively. While AA was effective at an extracellular concentration of 1 µM and an intracellular concentration of 1 pM, extracellular H2O2 was equally effective only at a concentration >800 µM (0.0027%). In contrast to AA, H2O2 decreased the slope of activation and increased the slope of inactivation of IA and reduced the sustained delayed rectifier current IK(V) by 22% and shifted its activation by -9 mV. Intracellular application of the antioxidant glutathione (GSH, 2-5 mM) blocked all effects of AA and the reduction of IA by H2O2. In contrast, intracellular GSH enhanced reduction of IK(V) by H2O2. Decrease of the slope of activation and increase of the slope of inactivation of IA by hydrogen peroxide was blocked and reversed to a decrease, respectively, by intracellular application of GSH. Intracellular GSH did not prevent H2O2 to shift inactivation and activation of IA and activation of IK(V) to more negative potentials. We conclude, that AA and H2O2 modulate voltage-activated K currents differentially by oxidation of GSH accessible intracellular and GSH inaccessible extracellular K+-channel domains, thereby presumably affecting neuronal information processing and oxidative damage.




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