| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
We investigated roles for hydrogen sulfide, a possible novel gasotransmitter, in nociceptive processing, and obtained the following results :
1) Hyperalgesia caused by administration of hydrogen sulfide and L-cysteine
We first found that intraplantar (i.pl.) administration of NaHS, a donor for hydrogen sulfide, caused mechanical hyperalgesia in rats, an effect being mediated by activation of T-type calcium channels. Similarly, L-cysteine, an endogenous origin of hydrogen sulfide, when administered i.pl., produced hyperalgesia. This effect was considered to be mediated by production of endogenous hydrogen sulfide by cystathionine-gamma-lyase (CSE) from L-cysteine. The hyperalgesic effect of the hydrogen sulfide donor was accompanied by expression of Fos protein in the superficial layers of the spinal dorsal horn.
2) Facilitation by hydrogen sulfide of T-type calcium channel-mediated membrane currents in NG108-15 cells and mouse spinal dorsal root ganglion (DRG) neurons
We examined effect of hydrogen sulfide on functions of T-type calcium channels by determining barium currents using the whole-cell-patch-clamp method, and found that hydrogen sulfide facilitated T-type calcium channel-mediated membrane currents on NG108-15 cells and mouse DRG neurons.
3) Visceral pain caused by colonic luminal hydrogen sulfide in mice
Intracolonic administration of NaHS, a donor it hydrogen sulfide, caused visceral pain-like nociceptive behavior and referred abdominal hyperalgesia in mice, accompanied by phosphorylation of ERK in nociceptive neurons present in the superficial layers of the spinal dorsal horn.
Together, our study strongly suggests that endogenous hydrogen sulfide plays a role as a novel messenger in nociceptive processing.
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