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Hydrogen Sulfide Induces Hyperalgesia Through potentiation of NMDA receptors
Author(s) -
Wang XiuLi,
Zhao Xiaonan,
Liu Peng,
Li DePei,
Guo YueXian
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb733
Subject(s) - chemistry , nmda receptor , nociception , hyperalgesia , spinal cord , dorsal root ganglion , pharmacology , long term potentiation , sodium hydrosulfide , endogeny , neuropathic pain , receptor , anesthesia , hydrogen sulfide , neuroscience , medicine , biochemistry , biology , sulfur , organic chemistry
Hydrogen sulfide (H2S), is an endogenous neurotrasmitter, modulates various physiological and pathological events including nociception. In this study, we investigated the role of NMDA receptors in the nociception induced by H2S in spinal cord. Intraplantar injection of an H2S donor, NaHS, into hindpaw significantly decreased the paw withdrawal threshold (PWT) latency in the contralateral hindpaw. Furthermore, NR2B mRNA and protein levels were increased in the spinal dorsal horn, but not in dorsal root ganglion (DRG) in rats subjected to NaHS intraplantar injection. Intrathecal (i.t.) injection of methemoglobin, a H2S scavenger, blocked reduction of PWT and increases expression of NR2B mRNA induced by intraplantar injection of NaHS. In addition, NaHS‐induced alteration of PWT and NR2B expression was partly, but significantly, attenuated by intrathecal injection of hydroxylamine, a CBS inhibitor, Collectively, these data suggest that peripheral administration of H2S donor causes hyperalgesia through increase in NR2B expression and production of endogenous H2S in the spinal dorsal horn.