Non-peptidergic nociceptive neurons are essential for mechanical inflammatory hypersensitivity in mice

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dc.contributorLEDS - Laboratório de Dor e Sinalizaçãopt_BR
dc.contributor.authorPinto, Larissa G.pt_BR
dc.contributor.authorSouza, Guilherme R.pt_BR
dc.contributor.authorSant´Anna, Morena Brazil Martinspt_BR
dc.contributor.authorKusuda, Ricardopt_BR
dc.contributor.authorLopes, Alexandre H.pt_BR
dc.contributor.authorCunha, Fernando Q.pt_BR
dc.contributor.authorFerreira, Sérgio H.pt_BR
dc.contributor.authorCunha, Thiago M.pt_BR
dc.date.accessioned2020-07-09T21:24:40Z-
dc.date.available2020-07-09T21:24:40Z-
dc.date.issued2019pt_BR
dc.identifier.citationPinto LG., Souza GR., Sant´Anna MBM, Kusuda R, Lopes AH., Cunha FQ., et al. Non-peptidergic nociceptive neurons are essential for mechanical inflammatory hypersensitivity in mice. Mol Neurobiol. 2019 Aug;56(8):5715-5728. doi:10.1007/s12035-019-1494-5.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2801-
dc.description.abstractSmall nerve fibers that bind the isolectin B4 (IB4+ C-fibers) are a subpopulation of primary afferent neurons that are involved in nociceptive sensory transduction and do not express the neuropeptides substance P and calcitonin-gene related peptide (CGRP). Several studies have attempted to elucidate the functional role of IB4+-nociceptors in different models of pain. However, a functional characterization of the non-peptidergic nociceptors in mediating mechanical inflammatory hypersensitivity in mice is still lacking. To this end, in the present study, the neurotoxin IB4-Saporin (IB4-Sap) was employed to ablate non-peptidergic C-fibers. Firstly, we showed that intrathecal (i.t.) administration of IB4-Sap in mice depleted non-peptidergic C-fibers, since it decreased the expression of purinoceptor 3 (P2X3) and transient receptor potential cation channel subfamily V member 1 (TRPV1) in the dorsal root ganglia (DRGs) as well as IB4 labelling in the spinal cord. Non-peptidergic C-fibers depletion did not alter the mechanical nociceptive threshold, but it inhibited the mechanical inflammatory hypersensitivity induced by glial cell-derived neurotrophic factor (GDNF), but not nerve growth factor (NGF). Depletion of non-peptidergic C-fibers abrogated mechanical inflammatory hypersensitivity induced by carrageenan. Finally, it was found that the inflammatory mediators PGE2 and epinephrine produced a mechanical inflammatory hypersensitivity that was also blocked by depletion of non-peptidergic C-fibers. These data suggest that IB4-positive nociceptive nerve fibers are not involved in normal mechanical nociception but are sensitised by inflammatory stimuli and play a crucial role in mediating mechanical inflammatory hypersensitivity.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.format.extentp. 5715-5728pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofMolecular Neurobiologypt_BR
dc.titleNon-peptidergic nociceptive neurons are essential for mechanical inflammatory hypersensitivity in micept_BR
dc.typeArticlept_BR
dc.identifier.doi10.1007/s12035-019-1494-5pt_BR
dc.identifier.urlhttps://doi.org/10.1007/s12035-019-1494-5pt_BR
dc.contributor.externalKing’s College London¦¦Inglaterrapt_BR
dc.contributor.externalUniversidade de São Paulo (USP)¦¦Brasilpt_BR
dc.identifier.citationvolume56pt_BR
dc.identifier.citationissue8pt_BR
dc.subject.keywordNon-peptidergic C-fiberspt_BR
dc.subject.keywordIB4-saporinpt_BR
dc.subject.keywordMechanical hypersensitivitypt_BR
dc.subject.keywordInflammatory painpt_BR
dc.subject.keywordNociceptorspt_BR
dc.subject.keywordMicept_BR
dc.relation.ispartofabbreviatedMol Neurobiolpt_BR
dc.identifier.citationabntv. 56, n. 8, p. 5715-5728, ago. 2019pt_BR
dc.identifier.citationvancouver2019 Aug;56(8):5715-5728pt_BR
dc.contributor.butantanSant'Anna, Morena Brazil Martins|:Aluno|:LEDS - Laboratório de Dor e Sinalização|:pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦485177/2012-9pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2011/19670–0pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/08216–2pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2010/04043-8.pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
item.openairetypeArticle-
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item.grantfulltextembargo_29990101-
item.languageiso639-1English-
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