Hydrogen sulfide as a novel nociceptive messenger

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• 作者：Atsufumi Kawabata ; Tsuyoshi Ishiki ; Keita Nagasawa ; Shigeru Yoshida ; Yumi Maeda ; Tomoko Takahashi ; Fumiko Sekiguchi ; Tetsuyuki Wada ; Seiji Ichida ; Hiroyuki Nishikawa
• 关键词：Hydrogen sulfide ; T-type Ca²⁺ channel ; Hyperalgesia ; Pain ; Nociception ; Gasotransmitter
• 刊名：Pain
• 出版年：2007
• 出版时间：November 2007
• 年：2007
• 卷：132
• 期：1-2
• 页码：74-81
• 全文大小：634 K

文摘

Hydrogen sulfide (H₂S), an endogenous gasotransmitter, modulates various biological events such as inflammation in the mammalian body. The present study investigated possible involvement of H₂S in peripheral nociceptive processing. Intraplantar (i.pl.) administration of NaHS, a H₂S donor, produced prompt hyperalgesia in rats, accompanied by expression of Fos in the spinal dorsal horn. The H₂S-evoked hyperalgesia was blocked by 5,5′-dithio-bis-(2-nitrobenzoic acid) (DTNB), an oxidizing agent, or ethosuximide and mibefradil, T-type Ca²⁺ channel inhibitors. l-Cysteine, an endogenous source for H₂S, given i.pl., also elicited hyperalgesia, an effect being abolished by dl-propargylglycine (PPG) and β-cyanoalanine (BCA), inhibitors of cystathionine-γ-lyase, a H₂S synthesizing enzyme. PPG and/or BCA partially inhibited the hyperalgesia induced by i.pl. lipopolysaccharide, an effect being reversed by i.pl. NaHS. In the patch-clamp study using undifferentiated NG108-15 cells that express T-type, but not other types, of Ca²⁺ channels, NaHS enhanced the currents through the T-type channels, an effect being blocked by DTNB. Thus, H₂S appears to function as a novel nociceptive messenger through sensitization of T-type Ca²⁺ channels in the peripheral tissues, particularly during inflammation.