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Altered Excitability of Intestinal Neurons in Primary Culture Caused by Acute Oxidative Stress

Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3010, Australia

Submitted 4 November 2002; accepted in final form 21 January 2003

Neurons were isolated from the intestine of guinea pigs and grown in primary culture for 15 days. Using conventional whole cell recording techniques, we demonstrated that the majority of neurons express a prolonged poststimulus afterhyperpolarization (slow AHP). These neurons also had large-amplitude (100 mV), broad-duration (2 ms) action potentials and generated a hyperpolarization activated inward current (I_h). Application of H₂O₂ (0.22–8.8 mM) hyperpolarized these neurons but not those lacking slow AHPs. The H₂O₂-induced hyperpolarization was followed by irreversible depolarization at higher concentrations (more than 1 mM) of H₂O₂ while it was maintained after washout of submillimolar H₂O₂. The ionic mechanisms underlying the hyperpolarization included the suppression of I_h and the activation of an inwardly rectifying outward current, which was blocked by glybenclamide (25–50 µM) and TEA (30 mM). In addition, H₂O₂ suppressed the slow AHP and its underlying current. Internal perfusion of catalase and glutathione opposed the H₂O₂-mediated decrease in I_sAHP. Our results indicate that acute oxidative stress has neuron- and conductance-specific actions in intestinal neurons that may underlie pathophysiological conditions.