Advanced search
Start date
Betweenand
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

P2X3 receptors contribute to muscle pain induced by static contraction by a mechanism dependent on neutrophil migration

Full text
Author(s):
Aquino, Bruna de Melo [1] ; da Silva dos Santos, Diogo Francisco [1] ; Jorge, Carolina Ocanha [1] ; Salgado Marques, Aline Carolina [1] ; Teixeira, Juliana Maia [2] ; Parada, Carlos Amilcar [2] ; Goncalves Oliveira-Fusaro, Maria Claudia [1]
Total Authors: 7
Affiliation:
[1] Univ Estadual Campinas, Sch Appl Sci, Lab Pain & Inflammat Res, Pedro Zaccaria 1300, Limeira, SP - Brazil
[2] Univ Estadual Campinas, Inst Biol, Dept Struct & Funct Biol, Monteiro Lobato 255, Campinas, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: PURINERGIC SIGNALLING; v. 15, n. 2, p. 167-175, JUN 2019.
Web of Science Citations: 1
Abstract

P2X3 receptors are involved with several pain conditions. Muscle pain induced by static contraction has an important socioeconomic impact. Here, we evaluated the involvement of P2X3 receptors on mechanical muscle hyperalgesia and neutrophil migration induced by static contraction in rats. Also, we evaluated whether static contraction would be able to increase muscle levels of TNF-alpha and IL-1 beta. Male Wistar rats were pretreated with the selective P2X3 receptor antagonist, A-317491, by intramuscular or intrathecal injection and the static contraction-induced mechanical muscle hyperalgesia was evaluated using the Randall-Selitto test. Neutrophil migration was evaluated by measurement of myeloperoxidase (MPO) kinetic-colorimetric assay and the cytokines TNF-alpha and IL-1 beta by enzyme-linked immunosorbent assay. Intramuscular or intrathecal pretreatment with A-317491 prevented static contraction-induced mechanical muscle hyperalgesia. In addition, A-317491 reduced static contraction-induced mechanical muscle hyperalgesia when administered 30 and 60min of the beginning of static contraction, but not after 30 and 60min of the end of static contraction. Intramuscular A-317491 also prevented static contraction-induced neutrophil migration. In a period of 24h, static contraction did not increase muscle levels of TNF-alpha and IL-1 beta. These findings demonstrated that mechanical muscle hyperalgesia and neutrophil migration induced by static contraction are modulated by P2X3 receptors expressed on the gastrocnemius muscle and spinal cord dorsal horn. Also, we suggest that P2X3 receptors are important to the development but not to maintenance of muscle hyperalgesia. Therefore, P2X3 receptors can be pointed out as a target to musculoskeletal pain conditions induced by daily or work-related activities. (AU)

FAPESP's process: 12/10402-6 - Involvement of inflammatory mediators and of P2X3 receptors on muscle hyperalgesia induced by sustained isometric contraction in rats
Grantee:Bruna de Melo Aquino
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 13/23448-7 - Involvement of the central nervous system receptors in muscle hyperalgesia: role of P2X3, AMPA and NMDA receptors
Grantee:Aline Carolina Salgado Marques
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 11/11064-4 - Development of a new model for the study of muscle hyperalgesia and the involvement of P2X3 and P2X2/3 receptors in muscle hyperalgesia
Grantee:Maria Cláudia Gonçalves de Oliveira
Support Opportunities: Research Grants - Young Investigators Grants