title: Hydrogen sulfide induced disruption of Na+ homeostasis in the cortex.
abstract: Maintenance of ionic balance is essential for neuronal functioning. Hydrogen sulfide (H(2)S), 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 H(2)S 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 H(2)S 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 H(2)S-induced Na(+) influx, suggesting that H(2)S-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.
authors.affiliation: The Vivan L. Smith Department of Neurosurgery, The University of Texas Medical School at Houston, Houston, Texas 77030, USA.
authors.forename: Dongman
authors.initials: D
authors.lastname: Chao
authors.forename: Xiaozhou
authors.initials: X
authors.lastname: He
authors.forename: Yilin
authors.initials: Y
authors.lastname: Yang
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Balboni
authors.forename: Severo
authors.initials: S
authors.lastname: Salvadori
authors.forename: Dong H
authors.initials: DH
authors.lastname: Kim
authors.forename: Ying
authors.initials: Y
authors.lastname: Xia
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects*; D006862:Hydrogen Sulfide / Q000633:toxicity*; D066298:In Vitro Techniques; D017136:Ion Transport; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017470:Receptors, Glutamate / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D017470:Receptors, Glutamate; D012964:Sodium; D006862:Hydrogen Sulfide