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dc.contributor.authorPereira, Elizete Maria Rita-
dc.contributor.authorSouza, Jéssica Mabelle-
dc.contributor.authorCarobin, Natália Virtude-
dc.contributor.authorSilva, Juliana Figueira da-
dc.contributor.authorAstoni, Duana Carvalho dos Santos-
dc.contributor.authorSilva Júnior, Cláudio Antônio da-
dc.contributor.authorBinda, Nancy Scardua-
dc.contributor.authorBorges, Marcia Helena-
dc.contributor.authorNagem, Ronaldo Alves Pinto-
dc.contributor.authorKushmerick, Christopher-
dc.contributor.authorFerreira, Juliano-
dc.contributor.authorCastro Junior, Célio José de-
dc.contributor.authorRibeiro, Fabiola Mara-
dc.contributor.authorGomez, Marcus Vinicius-
dc.identifier.citationPEREIRA, E. M. R. et al. Phoneutria toxin PnTx3-5 inhibits TRPV1 channel with antinociceptive action in an orofacial pain model. Neuropharmacology, v. 162, p. 107826, jan. 2020. Disponível em: <>. Acesso em: 10 fev. 2020.pt_BR
dc.description.abstractCapsaicin, an agonist of TRPV1, evokes intracellular [Ca2+] transients and glutamate release from perfused trigeminal ganglion. The spider toxin PnTx3-5, native or recombinant is more potent than the selective TRPV1 blocker SB-366791 with IC50 of 47 ± 0.18 nM, 45 ± 1.18 nM and 390 ± 5.1 nM in the same experimental conditions. PnTx3-5 is thus more potent than the selective TRPV1 blocker SB-366791. PnTx3-5 (40 nM) and SB-366791 (3 μM) also inhibited the capsaicin-induced increase in intracellular Ca2+ in HEK293 cells transfected with TRPV1 by 75 ± 16% and 84 ± 3.2%, respectively. In HEK293 cells transfected with TRPA1, cinnamaldehyde (30 μM) generated an increase in intracellular Ca2+ that was blocked by the TRPA1 antagonist HC-030031 (10 μM, 89% inhibition), but not by PnTx3-5 (40 nM), indicating selectivity of the toxin for TRPV1. In whole-cell patch-clamp experiments on HEK293 cells transfected with TRPV1, capsaicin (10 μM) generated inward currents that were blocked by SB-366791 and by both native and recombinant PnTx3-5 by 47 ± 1.4%; 54 ± 7.8% and 56 ± 9.0%, respectively. Intradermal injection of capsaicin into the rat left vibrissa induced nociceptive behavior that was blocked by pre-injection with either SB-366791 (3 nmol/site i.d., 83.3 ± 7.2% inhibition) or PnTx3-5 (100 fmol/site, 89 ± 8.4% inhibition). We conclude that both native and recombinant PnTx3-5 are potent TRPV1 receptor antagonists with antinociceptive action on pain behavior evoked by capsaicin.pt_BR
dc.titlePhoneutria toxin PnTx3-5 inhibits TRPV1 channel with antinociceptive action in an orofacial pain model.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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