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Nociceptin/orphanin FQ receptor modulates painful and fatigue symptoms in a mouse model of fibromyalgia.
Pain 2019; 160(6):1383-1401PAIN

Abstract

Generalized pain and fatigue are both hallmarks of fibromyalgia, a syndrome with an indefinite etiology. The treatment options for fibromyalgia are currently limited, probably because of its intricate pathophysiology. Thus, further basic and clinical research on this condition is currently needed. This study investigated the effects of nociceptin/orphanin FQ (N/OFQ) receptor (NOPr) ligands and the modulation of the NOP system in the preclinical mouse model of reserpine-induced fibromyalgia. The effects of administration of the natural agonist N/OFQ and the selective NOPr antagonists (UFP-101 and SB-612111) were evaluated in fibromyalgia-related symptoms in reserpine-treated mice. The expression of prepronociceptin/orphanin FQ and NOPr was assessed in central and peripheral sites at different time points after reserpine administration. Nociceptin/orphanin FQ displayed dual effects in the behavioral changes in the reserpine-elicited fibromyalgia model. The peptide NOPr antagonist UFP-101 produced analgesic and antifatigue effects, by preventing alterations in brain activity and skeletal muscle metabolism, secondary to fibromyalgia induction. The nonpeptide NOPr antagonist SB-612111 mirrored the favorable effects of UFP-101 in painful and fatigue alterations induced by reserpine. A time-related up- or downregulation of prepronociceptin/orphanin FQ and NOPr was observed in supraspinal, spinal, and peripheral sites of reserpine-treated mice. Our data shed new lights on the mechanisms underlying the fibromyalgia pathogenesis, supporting a role for N/OFQ-NOP receptor system in this syndrome.

Authors+Show Affiliations

Escola de Ciências, Programa de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências da Saúde, Centro de Pesquisa em Toxicologia e Farmacologia, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Escola de Medicina, Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Escola de Medicina, Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Escola de Ciências, Programa de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências, Laboratório de Biologia Genômica e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Centro de Pesquisa Pré-Clínica, Instituto do Cérebro do Rio Grande do Sul, Brain Institute (BraIns), Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Centro de Pesquisa Pré-Clínica, Instituto do Cérebro do Rio Grande do Sul, Brain Institute (BraIns), Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências da Saúde, Curso de Graduação em Biomedicina, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Centro de Pesquisa Pré-Clínica, Instituto do Cérebro do Rio Grande do Sul, Brain Institute (BraIns), Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Escola de Ciências, Programa de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Medicina, Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências, Laboratório de Biologia Genômica e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.Escola de Ciências, Programa de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências da Saúde, Centro de Pesquisa em Toxicologia e Farmacologia, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Medicina, Programa de Pós-Graduação em Medicina e Ciências da Saúde, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. Escola de Ciências da Saúde, Programa de Pós-Graduação em Odontologia, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30720581

Citation

Dagnino, Ana Paula Aquistapase, et al. "Nociceptin/orphanin FQ Receptor Modulates Painful and Fatigue Symptoms in a Mouse Model of Fibromyalgia." Pain, vol. 160, no. 6, 2019, pp. 1383-1401.
Dagnino APA, da Silva RBM, Chagastelles PC, et al. Nociceptin/orphanin FQ receptor modulates painful and fatigue symptoms in a mouse model of fibromyalgia. Pain. 2019;160(6):1383-1401.
Dagnino, A. P. A., da Silva, R. B. M., Chagastelles, P. C., Pereira, T. C. B., Venturin, G. T., Greggio, S., ... Campos, M. M. (2019). Nociceptin/orphanin FQ receptor modulates painful and fatigue symptoms in a mouse model of fibromyalgia. Pain, 160(6), pp. 1383-1401. doi:10.1097/j.pain.0000000000001513.
Dagnino APA, et al. Nociceptin/orphanin FQ Receptor Modulates Painful and Fatigue Symptoms in a Mouse Model of Fibromyalgia. Pain. 2019;160(6):1383-1401. PubMed PMID: 30720581.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nociceptin/orphanin FQ receptor modulates painful and fatigue symptoms in a mouse model of fibromyalgia. AU - Dagnino,Ana Paula Aquistapase, AU - da Silva,Rodrigo Braccini Madeira, AU - Chagastelles,Pedro Cesar, AU - Pereira,Talita Carneiro Brandão, AU - Venturin,Gianina Teribele, AU - Greggio,Samuel, AU - Costa da Costa,Jaderson, AU - Bogo,Maurício Reis, AU - Campos,Maria Martha, PY - 2019/2/6/pubmed PY - 2019/2/6/medline PY - 2019/2/6/entrez SP - 1383 EP - 1401 JF - Pain JO - Pain VL - 160 IS - 6 N2 - Generalized pain and fatigue are both hallmarks of fibromyalgia, a syndrome with an indefinite etiology. The treatment options for fibromyalgia are currently limited, probably because of its intricate pathophysiology. Thus, further basic and clinical research on this condition is currently needed. This study investigated the effects of nociceptin/orphanin FQ (N/OFQ) receptor (NOPr) ligands and the modulation of the NOP system in the preclinical mouse model of reserpine-induced fibromyalgia. The effects of administration of the natural agonist N/OFQ and the selective NOPr antagonists (UFP-101 and SB-612111) were evaluated in fibromyalgia-related symptoms in reserpine-treated mice. The expression of prepronociceptin/orphanin FQ and NOPr was assessed in central and peripheral sites at different time points after reserpine administration. Nociceptin/orphanin FQ displayed dual effects in the behavioral changes in the reserpine-elicited fibromyalgia model. The peptide NOPr antagonist UFP-101 produced analgesic and antifatigue effects, by preventing alterations in brain activity and skeletal muscle metabolism, secondary to fibromyalgia induction. The nonpeptide NOPr antagonist SB-612111 mirrored the favorable effects of UFP-101 in painful and fatigue alterations induced by reserpine. A time-related up- or downregulation of prepronociceptin/orphanin FQ and NOPr was observed in supraspinal, spinal, and peripheral sites of reserpine-treated mice. Our data shed new lights on the mechanisms underlying the fibromyalgia pathogenesis, supporting a role for N/OFQ-NOP receptor system in this syndrome. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/30720581/Nociceptin/orphanin_FQ_receptor_modulates_painful_and_fatigue_symptoms_in_a_mouse_model_of_fibromyalgia_ L2 - http://Insights.ovid.com/pubmed?pmid=30720581 DB - PRIME DP - Unbound Medicine ER -