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The involvement of the TRPA1 receptor in a mouse model of sympathetically maintained neuropathic pain.
Eur J Pharmacol. 2015 Jan 15; 747:105-13.EJ

Abstract

Sympathetic fibres maintain some forms of neuropathic pain, but the underlying mechanisms are poorly understood. Therefore, this study investigated the possible involvement of transient receptor potential ankyrin 1 (TRPA1) and the role of the sympathetic nervous system (involved in sympathetically maintained neuropathic pain) in a model of neuropathic pain induced by sciatic nerve chronic constriction injury (CCI) in mice. Systemic injection of the selective TRPA1 antagonist HC-030031 reversed the mechanical and cold allodynia that was induced by sciatic nerve chronic constriction injury (CCI). Nerve injury also sensitised mice to nociception, which was induced by the intraplantar injection of a low dose of the TRPA1 agonist allyl isothiocyanate without changing TRPA1 immunoreactivity in the injected paw. Furthermore, chemical sympathectomy produced by guanethidine largely prevented CCI-induced mechanical and cold allodynia. CCI also induced a norepinephrine-triggered nociception that was inhibited by an α-adrenoceptor antagonist, norepinephrine transporter block and monoamine oxidase inhibition. Finally, the peripheral injection of HC-030031 also largely reduced CCI-induced norepinephrine nociception and mechanical or cold allodynia. Taken together, the present findings reveal a critical role of TRPA1 in mechanical and cold hypersensitivity and norepinephrine hypersensitivity following nerve injury. Finally, our results suggest that TRPA1 antagonism may be useful to treat patients who present sympathetically maintained neuropathic pain.

Authors+Show Affiliations

Graduate Program in Pharmacology, Department of Physiology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Pharmacology, Department of Physiology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Pharmacology, Department of Physiology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Department of Pharmaceutical Chemistry, University of Ferrara, Ferrara, Italy.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Graduate Program in Health Sciences, University of the Extreme South of Santa Catarina, Criciúma, SC, Brazil.Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.Department of Health Sciences, Clinical Pharmacology and Oncology Unit, University of Florence, Florence, Italy.Graduate Program in Pharmacology, Department of Physiology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Graduate Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Graduate Program in Pharmacology, Department of Pharmacology, Federal University of Santa Catarina,Florianópolis, SC, Brazil. Electronic address: ferreiraj99@gmail.com.Graduate Program in Pharmacology, Department of Physiology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Graduate Program in Pharmacology, Department of Pharmacology, Federal University of Paraná, Curitiba, PR, Brazil.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25498793

Citation

Pinheiro, Francielle de Vargas, et al. "The Involvement of the TRPA1 Receptor in a Mouse Model of Sympathetically Maintained Neuropathic Pain." European Journal of Pharmacology, vol. 747, 2015, pp. 105-13.
Pinheiro Fde V, Villarinho JG, Silva CR, et al. The involvement of the TRPA1 receptor in a mouse model of sympathetically maintained neuropathic pain. Eur J Pharmacol. 2015;747:105-13.
Pinheiro, F. d. e. . V., Villarinho, J. G., Silva, C. R., Oliveira, S. M., Pinheiro, K. d. e. . V., Petri, D., Rossato, M. F., Guerra, G. P., Trevisan, G., Antonello Rubin, M., Geppetti, P., Ferreira, J., & André, E. (2015). The involvement of the TRPA1 receptor in a mouse model of sympathetically maintained neuropathic pain. European Journal of Pharmacology, 747, 105-13. https://doi.org/10.1016/j.ejphar.2014.11.039
Pinheiro Fde V, et al. The Involvement of the TRPA1 Receptor in a Mouse Model of Sympathetically Maintained Neuropathic Pain. Eur J Pharmacol. 2015 Jan 15;747:105-13. PubMed PMID: 25498793.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The involvement of the TRPA1 receptor in a mouse model of sympathetically maintained neuropathic pain. AU - Pinheiro,Francielle de Vargas, AU - Villarinho,Jardel Gomes, AU - Silva,Cássia Regina, AU - Oliveira,Sara Marchesan, AU - Pinheiro,Kelly de Vargas, AU - Petri,Delia, AU - Rossato,Mateus Fortes, AU - Guerra,Gustavo Petri, AU - Trevisan,Gabriela, AU - Antonello Rubin,Maribel, AU - Geppetti,Pierangelo, AU - Ferreira,Juliano, AU - André,Eunice, Y1 - 2014/12/10/ PY - 2014/08/24/received PY - 2014/11/04/revised PY - 2014/11/22/accepted PY - 2014/12/16/entrez PY - 2014/12/17/pubmed PY - 2015/10/27/medline KW - Adrenoceptor KW - Chronic constriction injury KW - Cold allodynia KW - Mechanical allodynia KW - Norepinephrine KW - TRPA1 antagonist SP - 105 EP - 13 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 747 N2 - Sympathetic fibres maintain some forms of neuropathic pain, but the underlying mechanisms are poorly understood. Therefore, this study investigated the possible involvement of transient receptor potential ankyrin 1 (TRPA1) and the role of the sympathetic nervous system (involved in sympathetically maintained neuropathic pain) in a model of neuropathic pain induced by sciatic nerve chronic constriction injury (CCI) in mice. Systemic injection of the selective TRPA1 antagonist HC-030031 reversed the mechanical and cold allodynia that was induced by sciatic nerve chronic constriction injury (CCI). Nerve injury also sensitised mice to nociception, which was induced by the intraplantar injection of a low dose of the TRPA1 agonist allyl isothiocyanate without changing TRPA1 immunoreactivity in the injected paw. Furthermore, chemical sympathectomy produced by guanethidine largely prevented CCI-induced mechanical and cold allodynia. CCI also induced a norepinephrine-triggered nociception that was inhibited by an α-adrenoceptor antagonist, norepinephrine transporter block and monoamine oxidase inhibition. Finally, the peripheral injection of HC-030031 also largely reduced CCI-induced norepinephrine nociception and mechanical or cold allodynia. Taken together, the present findings reveal a critical role of TRPA1 in mechanical and cold hypersensitivity and norepinephrine hypersensitivity following nerve injury. Finally, our results suggest that TRPA1 antagonism may be useful to treat patients who present sympathetically maintained neuropathic pain. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/25498793/The_involvement_of_the_TRPA1_receptor_in_a_mouse_model_of_sympathetically_maintained_neuropathic_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(14)00855-3 DB - PRIME DP - Unbound Medicine ER -