{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,26]],"date-time":"2026-04-26T17:48:16Z","timestamp":1777225696933,"version":"3.51.4"},"reference-count":37,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:p> Reactive oxygen species (ROS) modulate neuronal excitability. In the present study we examined the effects of hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>), a well established ROS, on neuronal activity from two neonatal mouse brain regions, i.e., the pre-B\u00f6tzinger complex (preB\u00f6tC) within the ventral respiratory column (VRC) and the CA1 area of the hippocampus. In the preB\u00f6tC, 2.2 mM H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> evoked a transient depression followed by augmentation of neuronal activity. The iron chelator deferoxamine (500 \u03bcM) did not prevent H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-mediated neuronal augmentation but prevented the initial depression. Combined application of Fe<jats:sup>2+<\/jats:sup> and H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> only caused depression of the preB\u00f6tC rhythm. In contrast, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> suppressed neuronal activity in the CA1 region, and this effect was accentuated by coapplication of Fe<jats:sup>2+<\/jats:sup> and H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, suggesting that hydroxyl radical generated by Fenton reaction mediates the effects of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> on CA1 neuronal activity. Malondialdehyde (MDA) levels were monitored as an index of lipid peroxidation in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated preB\u00f6tC and CA1 areas. MDA levels were unaltered in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated preB\u00f6tC, whereas MDA levels were markedly elevated in the CA1 region. These findings suggest that 1) exogenous administration of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> exerts differential effects on neuronal activities of preB\u00f6tC versus CA1 neuronal populations and 2) H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> is a potent modulator of respiratory rhythmogenesis from the preB\u00f6tC without affecting global oxidative status. <\/jats:p>","DOI":"10.1152\/jn.00550.2010","type":"journal-article","created":{"date-parts":[[2011,8,17]],"date-time":"2011-08-17T22:02:47Z","timestamp":1313618567000},"page":"3045-3055","source":"Crossref","is-referenced-by-count":21,"title":["Hydrogen peroxide differentially affects activity in the pre-B\u00f6tzinger complex and hippocampus"],"prefix":"10.1152","volume":"106","author":[{"suffix":"III","given":"Alfredo J.","family":"Garcia","sequence":"first","affiliation":[{"name":"Center for Integrative Brain Research, Seattle Children's Research Institute and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shakil A.","family":"Khan","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of Oxygen Sensing, Department of Medicine, University of Chicago, Chicago, Illinois"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ganesh K.","family":"Kumar","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of Oxygen Sensing, Department of Medicine, University of Chicago, Chicago, Illinois"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nanduri R.","family":"Prabhakar","sequence":"additional","affiliation":[{"name":"Institute for Integrative Physiology and Center for Systems Biology of Oxygen Sensing, Department of Medicine, University of Chicago, Chicago, Illinois"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan-Marino","family":"Ramirez","sequence":"additional","affiliation":[{"name":"Center for Integrative Brain Research, Seattle Children's Research Institute and"},{"name":"Departments of Neurological Surgery and Pediatrics, University of Washington, Seattle, Washington; 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