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  • 1
    Online Resource
    Online Resource
    P2X7‐induced nociception in the temporomandibular joint of rats depends on inflammatory mechanisms and C‐fibres sensitization
    Wiley ; 2021
    In:  European Journal of Pain Vol. 25, No. 5 ( 2021-05), p. 1107-1118
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    In: European Journal of Pain, Wiley, Vol. 25, No. 5 ( 2021-05), p. 1107-1118
    Abstract: P2X7 receptors are responsible for triggering inflammatory responses contributing to processes of pain in articular tissues. This study aimed to investigate whether the activation of the P2X7 receptor located in the temporomandibular joint (TMJ) tissues induces nociception through an inflammatory mechanisms and/or the activation of C‐fibres (small‐diameter primary afferents) of rats’ TMJ. Methods The TMJ hypernociception induced by the activation of P2X7 receptor was assessed by measuring the behavioural nociceptive responses. After behavioural experiments, the animals were terminally anaesthetized and periarticular tissues were removed and homogenate for enzyme‐linked immunosorbent assay, leukocyte infiltration and western blotting analysis. Results The nonselective P2X7 receptor agonist BzATP induced a dose‐dependent TMJ nociception, which was blocked by the selective P2X7 receptor antagonist A‐438079. The co‐administration of the selective β2‐adrenoceptor antagonist (ICI‐118,551) and the pre‐treatment with cyclooxygenase inhibitor indomethacin or with the nonspecific selectin inhibitor Fucoidan significantly reduced BzATP‐induced TMJ nociception. BzATP also induced an increase of pro‐inflammatory cytokines TNFα, IL‐1β and CINC‐1 levels, as well as leukocyte recruitment in TMJ tissue, effects that were reduced by A‐438079. Moreover BzATP‐induced TMJ nociception was inhibited in rats neonatal‐treated with Capsaicin (depleting C‐fibers). Finally, BzATP‐induced an increase in TRPV1 expression in TMJ tissue. Conclusions These findings suggest that P2X7 receptor activation in TMJ of rats induces nociceptive responses mediated by sympathomimetic amines, prostaglandins, leukocyte migration and increased levels of pro‐inflammatory cytokines. Furthermore, the P2X7 receptor activation induces nociceptive responses dependent on the activation of the primary afferent nociceptors of rats’ TMJ. Significance The activation of P2X7 receptors has an essential role in TMJ nociception and could be an interesting target to control the inflammatory pain in temporomandibular disorders.
    Type of Medium: Online Resource
    ISSN: 1090-3801 , 1532-2149
    URL: Issue
    URL: Article
    DOI: 10.1002/ejp.v25.5
    DOI: 10.1002/ejp.1732
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2002493-9
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  • 2
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    Online Resource
    Inflammatory pain in peripheral tissue depends on the activation of the TNF‐α type 1 receptor in the primary afferent neuron
    Wiley ; 2021
    In:  European Journal of Neuroscience Vol. 53, No. 2 ( 2021-01), p. 376-389
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 53, No. 2 ( 2021-01), p. 376-389
    Abstract: The mechanism underlying the role of tumor necrosis factor alpha (TNF‐α) in the development of inflammatory hyperalgesia has been extensively studied, mainly the role of TNF‐α in the release of pro‐inflammatory cytokines. The current concept relies in the fact that TNF‐α stimulates the cascade release of other pro‐inflammatory cytokines, such as IL‐1β, IL‐6, and IL‐8 (CINC‐1 in rats), triggering the release of the final inflammatory mediator prostaglandin E 2 (PGE 2 ) and sympathetic amines that directly sensitize the nociceptors. However, this may not be the sole mechanism involved as the blockade of TNF‐α synthesis by thalidomide prevents hyperalgesia without interrupting the synthesis of IL‐1β, IL‐6, and CINC‐1. Therefore, we hypothesized that activation of TNF‐α receptor type 1 (TNFR1) by TNF‐α increases nociceptors’ susceptibility to the action of PGE 2 and dopamine. We have found out that intrathecal administration of oligodeoxynucleotide‐antisense (ODN‐AS) against TNFR1 or thalidomide prevented carrageenan‐induced hyperalgesia. The co‐administration of TNF‐α with a subthreshold dose of PGE 2 or dopamine that does not induce hyperalgesia by itself in the hind paw of Wistar rats pretreated with dexamethasone (to prevent the endogenous release of cytokines) induced a robust hyperalgesia that was prevented by intrathecal treatment with ODN‐AS against TNFR1. We consider that the activation of neuronal TNFR1 by TNF‐α decisively increases the susceptibility of the peripheral afferent neuron to the action of final inflammatory mediators – PGE 2 and dopamine – that ultimately induce hyperalgesia. This mechanism may also underlie the analgesic action of thalidomide.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    URL: Article
    DOI: 10.1111/ejn.v53.2
    DOI: 10.1111/ejn.14985
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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