#cparse("/super/config/super.config.vm") #cparse("/neuro/includes/site.config.fhtml")#cparse("${superIncludes}/super.before-doctype.fhtml") #set($articleDate = '20061119') #cparse("${superIncludes}/super.head-top.fhtml")#cparse("${directoryIncludes}/metalink.fhtml") Dynorphin A activates bradykinin receptors to maintain neuropathic pain : Abstract : $siteName #set($adZone = 'article') #set($artid = '') #set($issue = '12') #set($subjectcode = '') #set($channelcode = '') #set($keyword = "") #set($discipline = '') #set($region = '') #set($careerstg = '') #cparse("${directoryIncludes}/style.fhtml")#cparse("${superIncludes}/super.head-bottom.fhtml") #cparse("${superIncludes}/super.body-top.fhtml")#cparse("${directoryIncludes}/header.fhtml")

Article abstract

#cparse("${common}/includes/separator.fhtml")

$siteName 9, 1534 - 1540 (2006)
Published online: 19 November 2006 | doi:10.1038/nn1804

#cparse("/neuro/journal/v9/n12/errorcorr/nn1804_errcrr.fhtml")

Dynorphin A activates bradykinin receptors to maintain neuropathic pain

#cparse("/neuro/journal/v9/n12/snippets/nn1804-corres.fhtml")

Josephine Lai1, Miaw-Chyi Luo1, Qingmin Chen1, Shouwu Ma1, Luis R Gardell1, Michael H Ossipov1 & Frank Porreca1

#cparse("${common}/includes/separator.fhtml")

Dynorphin A is an endogenous opioid peptide that produces non-opioid receptor-mediated neural excitation. Here we demonstrate that dynorphin induces calcium influx via voltage-sensitive calcium channels in sensory neurons by activating bradykinin receptors. This action of dynorphin at bradykinin receptors is distinct from the primary signaling pathway activated by bradykinin and underlies the hyperalgesia produced by pharmacological administration of dynorphin by the spinal route in rats and mice. Blockade of spinal B1 or B2 receptor also reverses persistent neuropathic pain but only when there is sustained elevation of endogenous spinal dynorphin, which is required for maintenance of neuropathic pain. These data reveal a mechanism for endogenous dynorphin to promote pain through its agonist action at bradykinin receptors and suggest new avenues for therapeutic intervention.

#cparse("${common}/includes/global.backtotop.fhtml")#cparse("${common}/includes/separator.fhtml")
  1. Department of Pharmacology, University of Arizona Health Sciences Center, 1501 N. Campbell Ave., Tucson, Arizona 85724, USA.

Correspondence to: Josephine Lai1 e-mail: lai@u.arizona.edu



#cparse("/neuro/journal/v9/n12/autonomy/embed/nn1804.html")
#if ($isCurrentIssue) #set ($menuCurrentPage = "current_issue") #else #set ($menuCurrentPage = "archive") #end

Main navigation

#cparse("${directoryIncludes}/main_journal_links.fhtml")#cparse("${directoryIncludes}/supplementary_journal_links.fhtml")#cparse("${directoryIncludes}/npg_resources.fhtml")#cparse("${common}/includes/npg_subjectareas.fhtml")
#cparse("${common}/includes/separator.fhtml")

Extra navigation

#cparse("${directoryIncludes}/rh_marketing.fhtml")

See also

Search PubMed for

#cparse("/njobs/neuro.html")#cparse("${common}/includes/natureproducts.fhtml") #if($articleAssociation.hasArticleAssociation($request, $session)) #cparse("${common}/includes/ads/abad.fhtml")#else #cparse("${directoryIncludes}/ads/skyad.fhtml")#end
#cparse("${directoryIncludes}/footer.fhtml")#cparse("${superIncludes}/super.body-bottom.fhtml")