Journal Article

Hydrogen Sulfide Induced Disruption of Na<sup>+</sup> Homeostasis in the Cortex

Dongman Chao, Xiaozhou He, Yilin Yang, Gianfranco Balboni, Severo Salvadori, Dong H. Kim and Ying Xia

in Toxicological Sciences

Volume 128, issue 1, pages 198-208
Published in print July 2012 | ISSN: 1096-6080
Published online April 2012 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/kfs125
Hydrogen Sulfide Induced Disruption of Na+ Homeostasis in the Cortex

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Maintenance of ionic balance is essential for neuronal functioning. Hydrogen sulfide (H2S), a known toxic environmental gaseous pollutant, has been recently recognized as a gasotransmitter involved in numerous biological processes and is believed to play an important role in the neural activities under both physiological and pathological conditions. However, it is unclear if it plays any role in maintenance of ionic homeostasis in the brain under physiological/pathophysiological conditions. Here, we report by directly measuring Na+ activity using Na+ selective electrodes in mouse cortical slices that H2S donor sodium hydrosulfide (NaHS) increased Na+ influx in a concentration-dependent manner. This effect could be partially blocked by either Na+ channel blocker or N-methyl-D-aspartate receptor (NMDAR) blocker alone or almost completely abolished by coapplication of both blockers but not by non-NMDAR blocker. These data suggest that increased H2S in pathophysiological conditions, e.g., hypoxia/ischemia, potentially causes a disruption of ionic homeostasis by massive Na+ influx through Na+ channels and NMDARs, thus injuring neural functions. Activation of delta-opioid receptors (DOR), which reduces Na+ currents/influx in normoxia, had no effect on H2S-induced Na+ influx, suggesting that H2S-induced disruption of Na+ homeostasis is resistant to DOR regulation and may play a major role in neuronal injury in pathophysiological conditions, e.g., hypoxia/ischemia.

Keywords: hydrogen sulfide; Na+ homeostasis; ionotropic glutamate receptor; Na+ channel; delta-opioid receptor; cortex

Journal Article.  8133 words.  Illustrated.

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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