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The Journal of Neuroscience, March 12, 2008, 28(11):2856-2863; doi:10.1523/JNEUROSCI.4389-07.2008

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Neurobiology of Disease
Neuropathic Pain-Like Behavior after Brachial Plexus Avulsion in Mice: The Relevance of Kinin B₁ and B₂ Receptors

Nara L. M. Quintão,¹ Giselle F. Passos,¹ Rodrigo Medeiros,¹ Ana F. Paszcuk,¹ Fabiana L. Motta,³ João B. Pesquero,³ Maria M. Campos,² and João B. Calixto¹

¹Department of Pharmacology, Center of Biological Sciences, Universidade Federal de Santa Catarina, CEP 88049-900, Florianópolis, Brazil, ²School of Dentistry, Pontifícia Universidade Católica do Rio Grande do Sul, CEP 90169-900 Porto Alegre, Brazil, and ³Department of Biophysics, Universidade Federal de São Paulo-Escola Paulista de Medicina, CEP 04023-900 São Paulo, Brazil

Correspondence should be addressed to Dr. J. B. Calixto, Departamento de Farmacologia, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Bloco D, CCB, Caixa Postal 476, CEP 88049-900, Florianópolis, SC, Brazil. Email: calixto{at}farmaco.ufsc.br or Email: calixto3{at}terra.com.br

The relevance of kinin B₁ (B₁R) and B₂ (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 30 d after the BPA, whereas in the spinal cord, this parameter was augmented only at 4 d. The data provide new evidence 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.

Key words: mouse brachial plexus; neuropathic pain; hypernociception; kinins; B₁ receptor; B₂ receptor

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Received Sept. 25, 2007; revised Jan. 30, 2008; accepted Jan. 31, 2008.

Correspondence should be addressed to Dr. J. B. Calixto, Departamento de Farmacologia, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Bloco D, CCB, Caixa Postal 476, CEP 88049-900, Florianópolis, SC, Brazil. Email: calixto{at}farmaco.ufsc.br or Email: calixto3{at}terra.com.br

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