Reduced nerve injury-induced neuropathic pain in kinin B-1 receptor knock-out mice

Show simple item record Ferreira, Juliano Beirith, Alessandra Mori, Marcelo A S [UNIFESP] Araujo, Ronaldo C. Bader, Michael Pesquero, Joao Bosco [UNIFESP] Calixto, Joao B 2016-01-24T12:37:43Z 2016-01-24T12:37:43Z 2005-03-02
dc.identifier.citation Journal of Neuroscience. Washington: Soc Neuroscience, v. 25, n. 9, p. 2405-2412, 2005.
dc.identifier.issn 0270-6474
dc.description.abstract Injury to peripheral nerves often results in a persistent neuropathic pain condition that is characterized by spontaneous pain, allodynia, and hyperalgesia. Nerve injury is accompanied by a local inflammatory reaction in which nerve-associated and immune cells release several pronociceptive mediators. Kinin B-1 receptors are rarely expressed in nontraumatized tissues, but they can be expressed after tissue injury. Because B-1 receptors mediate chronic inflammatory painful processes, we studied their participation in neuropathic pain using receptor gene-deleted mice. in the absence of neuropathy, we found no difference in the paw-withdrawal responses to thermal or mechanical stimulation between B-1 receptor knock-out mice and 129/J wild-type mice. Partial ligation of the sciatic nerve in the wild-type mouse produced a profound and long-lasting decrease in thermal and mechanical thresholds in the paw ipsilateral to nerve lesion. Threshold changed neither in the sham-operated animals nor in the paw contralateral to lesion. Ablation of the gene for the B-1 receptor resulted in a significant reduction in early stages of mechanical allodynia and thermal hyperalgesia. Furthermore, systemic treatment with the B-1 selective receptor antagonist des-Arg(9)-[Leu(8)]-bradykinin reduced the established mechanical allodynia observed 7-28d after nerve lesion in wild-type mice. Partial sciatic nerve ligation induced an upregulation in B-1 receptor mRNA in ipsilateral paw, sciatic nerve, and spinal cord of wild-type mice. Together, kinin B-1 receptor activation seems to be essential to neuropathic pain development, suggesting that an oral-selective B-1 receptor antagonist might have therapeutic potential in the management of chronic pain. en
dc.format.extent 2405-2412
dc.language.iso eng
dc.publisher Soc Neuroscience
dc.relation.ispartof Journal of Neuroscience
dc.rights Acesso aberto
dc.subject neuropathic pain en
dc.subject allodynia en
dc.subject hyperalgesia en
dc.subject B-1 receptor en
dc.subject kinin en
dc.subject bradykinin en
dc.title Reduced nerve injury-induced neuropathic pain in kinin B-1 receptor knock-out mice en
dc.type Artigo
dc.contributor.institution Universidade Federal de Santa Catarina (UFSC)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Univ Mogi Cruzes
dc.contributor.institution Max Delbruck Ctr Mol Med
dc.description.affiliation Univ Fed Santa Catarina, Dept Pharmacol, Ctr Biol Sci, BR-88049900 Florianopolis, SC, Brazil
dc.description.affiliation Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, Brazil
dc.description.affiliation Univ Mogi Cruzes, BR-0878091 Mogi Das Cruzes, Brazil
dc.description.affiliation Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany
dc.description.affiliationUnifesp Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, Brazil
dc.identifier.doi 10.1523/JNEUROSCI.2466-04.2005
dc.description.source Web of Science
dc.identifier.wos WOS:000227343800026


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