These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Chelating luminal zinc mimics hydrogen sulfide-evoked colonic pain in mice: possible involvement of T-type calcium channels.
    Author: Matsunami M, Kirishi S, Okui T, Kawabata A.
    Journal: Neuroscience; 2011 May 05; 181():257-64. PubMed ID: 21354272.
    Abstract:
    Luminal hydrogen sulfide (H(2)S) causes colonic pain and referred hyperalgesia in mice through activation of T-type Ca(2+) channels. To test a hypothesis that H(2)S might chelate and remove endogenous Zn(2+) that inhibits the Ca(v)3.2 isoform of T-type Ca(2+) channels, facilitating visceral nociception, we asked if intracolonic (i.col.) administration of Zn(2+) chelators mimics H(2)S-induced visceral nociception. Visceral nociceptive behavior and referred abdominal allodynia/hyperalgesia were determined after i.col. administration of NaHS, a donor for H(2)S, or Zn(2+) chelators in mice. Phospholylation of extracellular signal-regulated protein kinase (ERK) in the spinal cord was analyzed by immunohistochemistry. The visceral nociceptive behavior and referred abdominal allodynia/hyperalgesia caused by i.col. NaHS in mice were abolished by i.col. preadministration of zinc chloride (ZnCl(2)), known to selectively inhibit Ca(v)3.2, but not Ca(v)3.1 or Ca(v)3.3, isoforms of T-type Ca(2+) channels, and by i.p. preadministration of mibefradil, a pan-T-type Ca(2+) channel blocker. Two distinct Zn(2+) chelators, N,N,N',N'-tetrakis(2-pyridylmethyl)ehylenediamine (TPEN) and dipicolinic acid, when administered i.col., mimicked the NaHS-evoked visceral nociceptive behavior and referred abdominal allodynia/hyperalgesia, which were inhibited by mibefradil and by NNC 55-0396, another T-type Ca(2+) channel blocker. Like i.col. NaHS, i.col. TPEN caused prompt phosphorylation of ERK in the spinal dorsal horn, an effect blocked by mibefradil. Removal of luminal Zn(2+) by H(2)S and other Zn(2+) chelators thus produces colonic pain through activation of T-type Ca(2+) channels, most probably of the Ca(v)3.2 isoform. Hence, endogenous Zn(2+) is considered to play a critical role in modulating visceral pain.
    [Abstract] [Full Text] [Related] [New Search]