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Hydrogen peroxide differentially affects activity in the pre-Boetzinger complex and hippocampus

Reactive oxygen species (ROS) modulate neuronal excitability. In the present study we examined the effects of hydrogen peroxide (H2O2), a well established ROS, on neuronal activity from two neonatal mouse brain regions, i.e., the pre-Boetzinger complex (preBoetC) within the ventral respiratory colum...

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Bibliographic Details
Published in:Journal of neurophysiology 2011-01, Vol.106 (6), p.3045-3055
Main Authors: Garcia, Alfredo J, Khan, Shakil A, Kumar, Ganesh K, Prabhakar, Nanduri R, Ramirez, Jan-Marino
Format: Article
Language:English
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Summary:Reactive oxygen species (ROS) modulate neuronal excitability. In the present study we examined the effects of hydrogen peroxide (H2O2), a well established ROS, on neuronal activity from two neonatal mouse brain regions, i.e., the pre-Boetzinger complex (preBoetC) within the ventral respiratory column (VRC) and the CA1 area of the hippocampus. In the preBoetC, 2.2 mM H2O2 evoked a transient depression followed by augmentation of neuronal activity. The iron chelator deferoxamine (500 mu M) did not prevent H2O2-mediated neuronal augmentation but prevented the initial depression. Combined application of Fe2+ and H2O2 only caused depression of the preBoetC rhythm. In contrast, H2O2 suppressed neuronal activity in the CA1 region, and this effect was accentuated by coapplication of Fe2+ and H2O2, suggesting that hydroxyl radical generated by Fenton reaction mediates the effects of H2O2 on CA1 neuronal activity. Malondialdehyde (MDA) levels were monitored as an index of lipid peroxidation in H2O2-treated preBoetC and CA1 areas. MDA levels were unaltered in H2O2-treated preBoetC, whereas MDA levels were markedly elevated in the CA1 region. These findings suggest that 1) exogenous administration of H2O2 exerts differential effects on neuronal activities of preBoetC versus CA1 neuronal populations and 2) H2O2 is a potent modulator of respiratory rhythmogenesis from the preBoetC without affecting global oxidative status.
ISSN:0022-3077