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Hydrogen sulfide as a novel nociceptive messenger

Kawabata, Atsufumia,*; Ishiki, Tsuyoshia; Nagasawa, Keitaa; Yoshida, Shigerub; Maeda, Yumia; Takahashi, Tomokoa; Sekiguchi, Fumikoa; Wada, Tetsuyukic; Ichida, Seijic; Nishikawa, Hiroyukid

doi: 10.1016/j.pain.2007.01.026
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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.

aDivision of Physiology and Pathophysiology, Department of Pharmacy, School of Pharmacy, Kinki University, Higashi-Osaka 577-8502, Japan

bDepartment of Life Science, School of Science and Engineering, Kinki University, Higashi-Osaka 577-8502, Japan

cDivision of Biological Chemistry, Department of Pharmacy, School of Pharmacy, Kinki University, Higashi-Osaka 577-8502, Japan

dResearch and Development Center, Fuso Pharmaceutical Industries Ltd., Osaka 536-8523, Japan

*Corresponding author. Tel.: +81 6 6721 2332; fax: +81 6 6730 1394.

E-mail: kawabata@phar.kindai.ac.jp

Submitted August 31, 2006; received in revised form November 27, 2006; accepted January 29, 2007.

© 2007 Lippincott Williams & Wilkins, Inc.
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