Evidence for the role of neurogenic inflammation components in trypsin-elicited scratching behaviour in mice

Evidence for the role of neurogenic inflammation components in trypsin-elicited scratching behaviour in mice

Autor Costa, R. Google Scholar
Marotta, D. M. Google Scholar
Manjavachi, M. N. Google Scholar
Fernandes, E. S. Google Scholar
Lima-Garcia, J. F. Google Scholar
Paszcuk, A. F. Google Scholar
Quintao, N. L. M. Google Scholar
Juliano, Luiz Autor UNIFESP Google Scholar
Brain, S. D. Google Scholar
Calixto, J. B. Google Scholar
Instituição Universidade Federal de Santa Catarina (UFSC)
Universidade Federal de São Paulo (UNIFESP)
Kings Coll London
Resumo Background and purpose: We investigated the mechanisms underlying the pruritogenic response induced by trypsin in mice, to assess the relevance of neurogenic inflammation components in this response.Experimental approach: Itching was induced by an intradermal injection of trypsin in the mouse neck. the animals were observed for 40 min and their scratching behaviour was quantified.Key results: Trypsin-induced itching was blocked by the lima bean trypsin inhibitor, the selective proteinase-activated receptor-2 (PAR-2) antagonist FSLLRY and PAR-2 receptor desensitization. An important involvement of mast cells was observed, as chronic pretreatment with the mast cell degranulator compound 48/80 or the mast cell stabilizer disodium cromoglycate prevented scratching. Also, trypsin response was inhibited by the selective COX-2 inhibitor celecoxib and by the selective kinin B(2) (FR173657) and B(1) (SSR240612) receptor antagonists. Moreover, an essential role for the mediators of neurogenic inflammation was established, as the selective NK(1)(FK888), NK(3) (SR142801) and calcitonin gene-related peptide (CGRP(8-37) fragment) receptor antagonists inhibited trypsin-induced itching. Similarly, blockade of transient receptor potential vanilloid 1 (TRPV1) receptors by the selective TRPV1 receptor antagonist SB366791, or by genetic deletion of TRPV1 receptor reduced this behaviour in mice. C-fibre desensitization showed a very similar result.Conclusions and implications: Trypsin intradermal injection proved to be a reproducible model for the study of itching and the involvement of PAR-2 receptors. Also, trypsin-induced itching seems to be widely dependent on neurogenic inflammation, with a role for TRPV1 receptors. in addition, several other mediators located in the sensory nerves and skin also seem to contribute to this process.
Assunto trypsin
PAR-2
scratching behaviour
neuropeptides
TRPV1
mast cells
Idioma Inglês
Data 2008-07-01
Publicado em British Journal of Pharmacology. Malden: Wiley-Blackwell, v. 154, n. 5, p. 1094-1103, 2008.
ISSN 0007-1188 (Sherpa/Romeo, fator de impacto)
Editor Wiley-Blackwell
Extensão 1094-1103
Fonte http://dx.doi.org/10.1038/bjp.2008.172
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000257269400019
URI http://repositorio.unifesp.br/handle/11600/30743

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