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Luminal hydrogen sulfide plays a pro-nociceptive role in mouse colon
  1. Maho Matsunami
  1. Kinki University, Japan
    1. Takeshi Tarui
    1. Kinki University, Japan
      1. Kenji Mitani
      1. Kinki University, Japan
        1. Keita Nagasawa
        1. Kinki University, Japan
          1. Osamu Fukushima
          1. Kinki University, Japan
            1. Kazumasa Okubo
            1. Kinki University, Japan
              1. Shigeru Yoshida
              1. Kinki University, Japan
                1. Motohide Takemura
                1. Osaka University, Japan
                  1. Atsufuni Kawabata (kawabata{at}phar.kindai.ac.jp)
                  1. Kinki University, Japan

                    Abstract

                    Objective: Given our recent evidence that hydrogen sulfide (H2S), a gasotransmitter, promotes somatic pain through redox modulation of T-type Ca2+ channels, we examined roles for colonic luminal H2S in visceral nociceptive processing in mice.

                    Methods: After intracolonic (i.col.) administration of NaHS, a donor for H2S, visceral pain-like behavior and referred abdominal allodyina/hyperalgesia were evaluated. Phosphorylation of ERK in the spinal dorsal horn was determined immunohistochemically. The whole-cell recording technique was used to evaluate T-type Ca2+ currents (T-currents) in cultured dorsal root ganglion (DRG) neurons.

                    Results: Like capsaicin, NaHS, administered i.col. at 0.5-5 nmol/mouse, triggered visceral nociceptive behavior accompanied with referred allodynia/hyperalgesia in mice. Phosphorylation of ERK in the spinal dorsal horn was detected following i.col. NaHS or capsaicin. The behavioral effects of i.col. NaHS were abolished by a T-type channel blocker or an oxidant, but not inhibitors of L-type Ca2+ channels or ATP-sensitive K+ (KATP) channels. Intraperitoneal NaHS at 60 μmol/kg facilitated i.col. capsaicin-evoked visceral nociception, an effect being abolished by the T-type channel blocker, although it alone produced no behavioral effect. In DRG neurons, T-currents were enhanced by NaHS.

                    Conclusions: These findings suggest that colonic luminal H2S/NaHS plays pro-nociceptive roles, and imply that the underlying mechanisms might involve sensitization/activation of T-type channels probably in the primary afferents, aside from the issue of the selectivity of mibefradil.

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