Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/30527 http://dx.doi.org/10.1523/JNEUROSCI.4389-07.2008 |
Resumo: | The relevance of kinin B-1 (B1R) and B-2 (B2R) receptors in the brachial plexus avulsion (BPA) model was evaluated in mice, by means of genetic and pharmacological tools. BPA-induced hypernociception was absent in B1R, but not in B2R, knock-out mice. Local or intraperitoneal administration of the B2R antagonist Hoe 140 failed to affect BPA-induced mechanical hypernociception. Interestingly, local or intraperitoneal treatment with B1R antagonists, R-715 or SSR240612, dosed at the time of surgery, significantly reduced BPA-evoked mechanical hypernociception. Intrathecal or intracerebroventricular administration of these antagonists, at the surgery moment, did not prevent the hypernociception. Both antagonists, dosed by intraperitoneal or intrathecal routes (but not intracerebroventricularly) 4 d after the surgery, significantly inhibited the mechanical hypernociception. At 30 d after the BPA, only the intracerebroventricular treatment effectively reduced the hypernociception. A marked increase in B1R mRNA was observed in the hypothalamus, hippocampus, thalamus, and cortex at 4 d after BPA and only in the hypothalamus and cortex at 30 d. in the spinal cord, a slight increase in B1R mRNA expression was observed as early as at 2 d. Finally, an enhancement of B1R protein expression was found in all the analyzed brain structures at 4 and 30d after the BPA, whereas in the spinal cord, this parameter was augmented only at 4d. the data providenewevidence on the role of peripheral and central kinin B1R in the BPA model of neuropathic pain. Selective B1R antagonists might well represent valuable tools for the management of neuropathic pain. |
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Quintao, Nara L. M.Passos, Giselle F.Medeiros, RodrigoPaszcuk, Ana F.Motta, Fabiana L. [UNIFESP]Pesquero, Joao B. [UNIFESP]Campos, Maria M.Calixto, Joao B.Universidade Federal de Santa Catarina (UFSC)Pontificia Univ Catolica Rio Grande do SulUniversidade Federal de São Paulo (UNIFESP)2016-01-24T13:49:40Z2016-01-24T13:49:40Z2008-03-12Journal of Neuroscience. Washington: Soc Neuroscience, v. 28, n. 11, p. 2856-2863, 2008.0270-6474http://repositorio.unifesp.br/handle/11600/30527http://dx.doi.org/10.1523/JNEUROSCI.4389-07.200810.1523/JNEUROSCI.4389-07.2008WOS:000253973600022The relevance of kinin B-1 (B1R) and B-2 (B2R) receptors in the brachial plexus avulsion (BPA) model was evaluated in mice, by means of genetic and pharmacological tools. BPA-induced hypernociception was absent in B1R, but not in B2R, knock-out mice. Local or intraperitoneal administration of the B2R antagonist Hoe 140 failed to affect BPA-induced mechanical hypernociception. Interestingly, local or intraperitoneal treatment with B1R antagonists, R-715 or SSR240612, dosed at the time of surgery, significantly reduced BPA-evoked mechanical hypernociception. Intrathecal or intracerebroventricular administration of these antagonists, at the surgery moment, did not prevent the hypernociception. Both antagonists, dosed by intraperitoneal or intrathecal routes (but not intracerebroventricularly) 4 d after the surgery, significantly inhibited the mechanical hypernociception. At 30 d after the BPA, only the intracerebroventricular treatment effectively reduced the hypernociception. A marked increase in B1R mRNA was observed in the hypothalamus, hippocampus, thalamus, and cortex at 4 d after BPA and only in the hypothalamus and cortex at 30 d. in the spinal cord, a slight increase in B1R mRNA expression was observed as early as at 2 d. Finally, an enhancement of B1R protein expression was found in all the analyzed brain structures at 4 and 30d after the BPA, whereas in the spinal cord, this parameter was augmented only at 4d. the data providenewevidence on the role of peripheral and central kinin B1R in the BPA model of neuropathic pain. Selective B1R antagonists might well represent valuable tools for the management of neuropathic pain.Univ Fed Santa Catarina, Dept Pharmacol, Ctr Biol Sci, BR-88049900 Florianopolis, SC, BrazilPontificia Univ Catolica Rio Grande do Sul, Sch Dent, BR-90169900 Porto Alegre, RS, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023900 São Paulo, BrazilWeb of Science2856-2863engSoc NeuroscienceJournal of Neurosciencemouse brachial plexusneuropathic painhypernociceptionkininsB-1 receptorB-2 receptorNeuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptorsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/305272022-09-27 11:31:16.96metadata only accessoai:repositorio.unifesp.br:11600/30527Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:26:02.472489Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
title |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
spellingShingle |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors Quintao, Nara L. M. mouse brachial plexus neuropathic pain hypernociception kinins B-1 receptor B-2 receptor |
title_short |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
title_full |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
title_fullStr |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
title_full_unstemmed |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
title_sort |
Neuropathic pain-like behavior after brachial plexus avulsion in mice: the relevance of kinin B-1 and B-2 receptors |
author |
Quintao, Nara L. M. |
author_facet |
Quintao, Nara L. M. Passos, Giselle F. Medeiros, Rodrigo Paszcuk, Ana F. Motta, Fabiana L. [UNIFESP] Pesquero, Joao B. [UNIFESP] Campos, Maria M. Calixto, Joao B. |
author_role |
author |
author2 |
Passos, Giselle F. Medeiros, Rodrigo Paszcuk, Ana F. Motta, Fabiana L. [UNIFESP] Pesquero, Joao B. [UNIFESP] Campos, Maria M. Calixto, Joao B. |
author2_role |
author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de Santa Catarina (UFSC) Pontificia Univ Catolica Rio Grande do Sul Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Quintao, Nara L. M. Passos, Giselle F. Medeiros, Rodrigo Paszcuk, Ana F. Motta, Fabiana L. [UNIFESP] Pesquero, Joao B. [UNIFESP] Campos, Maria M. Calixto, Joao B. |
dc.subject.eng.fl_str_mv |
mouse brachial plexus neuropathic pain hypernociception kinins B-1 receptor B-2 receptor |
topic |
mouse brachial plexus neuropathic pain hypernociception kinins B-1 receptor B-2 receptor |
description |
The relevance of kinin B-1 (B1R) and B-2 (B2R) receptors in the brachial plexus avulsion (BPA) model was evaluated in mice, by means of genetic and pharmacological tools. BPA-induced hypernociception was absent in B1R, but not in B2R, knock-out mice. Local or intraperitoneal administration of the B2R antagonist Hoe 140 failed to affect BPA-induced mechanical hypernociception. Interestingly, local or intraperitoneal treatment with B1R antagonists, R-715 or SSR240612, dosed at the time of surgery, significantly reduced BPA-evoked mechanical hypernociception. Intrathecal or intracerebroventricular administration of these antagonists, at the surgery moment, did not prevent the hypernociception. Both antagonists, dosed by intraperitoneal or intrathecal routes (but not intracerebroventricularly) 4 d after the surgery, significantly inhibited the mechanical hypernociception. At 30 d after the BPA, only the intracerebroventricular treatment effectively reduced the hypernociception. A marked increase in B1R mRNA was observed in the hypothalamus, hippocampus, thalamus, and cortex at 4 d after BPA and only in the hypothalamus and cortex at 30 d. in the spinal cord, a slight increase in B1R mRNA expression was observed as early as at 2 d. Finally, an enhancement of B1R protein expression was found in all the analyzed brain structures at 4 and 30d after the BPA, whereas in the spinal cord, this parameter was augmented only at 4d. the data providenewevidence on the role of peripheral and central kinin B1R in the BPA model of neuropathic pain. Selective B1R antagonists might well represent valuable tools for the management of neuropathic pain. |
publishDate |
2008 |
dc.date.issued.fl_str_mv |
2008-03-12 |
dc.date.accessioned.fl_str_mv |
2016-01-24T13:49:40Z |
dc.date.available.fl_str_mv |
2016-01-24T13:49:40Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Journal of Neuroscience. Washington: Soc Neuroscience, v. 28, n. 11, p. 2856-2863, 2008. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/30527 http://dx.doi.org/10.1523/JNEUROSCI.4389-07.2008 |
dc.identifier.issn.none.fl_str_mv |
0270-6474 |
dc.identifier.doi.none.fl_str_mv |
10.1523/JNEUROSCI.4389-07.2008 |
dc.identifier.wos.none.fl_str_mv |
WOS:000253973600022 |
identifier_str_mv |
Journal of Neuroscience. Washington: Soc Neuroscience, v. 28, n. 11, p. 2856-2863, 2008. 0270-6474 10.1523/JNEUROSCI.4389-07.2008 WOS:000253973600022 |
url |
http://repositorio.unifesp.br/handle/11600/30527 http://dx.doi.org/10.1523/JNEUROSCI.4389-07.2008 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Journal of Neuroscience |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
2856-2863 |
dc.publisher.none.fl_str_mv |
Soc Neuroscience |
publisher.none.fl_str_mv |
Soc Neuroscience |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1783460290356051968 |