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Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist

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    SYSNO ASEP0542140
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleHypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist
    Author(s) Uchytilová, Eva (FGU-C)
    Špicarová, Diana (FGU-C) RID, ORCID
    Paleček, Jiří (FGU-C) RID, ORCID
    Article number3712
    Source TitleInternational Journal of Molecular Sciences. - : MDPI
    Roč. 22, č. 7 (2021)
    Number of pages12 s.
    Languageeng - English
    CountryCH - Switzerland
    KeywordsTRPV1 ; bradykinin ; OLDA ; spinal cord ; hyperalgesia ; allodynia
    Subject RIVFH - Neurology
    OECD categoryNeurosciences (including psychophysiology
    R&D ProjectsGA20-19136S GA ČR - Czech Science Foundation (CSF)
    Method of publishingOpen access
    Institutional supportFGU-C - RVO:67985823
    UT WOS000638655100001
    EID SCOPUS85103479134
    DOI10.3390/ijms22073712
    AnnotationTransient receptor potential vanilloid 1 (TRPV1) channels contribute to the development of several chronic pain states and represent a possible therapeutic target in many painful disease treatment. Proinflammatory mediator bradykinin (BK) sensitizes TRPV1, whereas noxious peripheral stimulation increases BK level in the spinal cord. Here, we investigated the involvement of spinal TRPV1 in thermal and mechanical hypersensitivity, evoked by intrathecal (i.t.) administration of BK and an endogenous agonist of TRPV1, N-oleoyldopamine (OLDA), using behavioral tests and i.t. catheter implantation, and administration of BK-induced transient thermal and mechanical hyperalgesia and mechanical allodynia. All these hypersensitive states were enhanced by co-administration of a low dose of OLDA (0.42 mu g i.t.), which was ineffective only under the control conditions. Intrathecal pretreatment with TRPV1 selective antagonist SB366791 prevented hypersensitivity induced by i.t. co-administration of BK and OLDA. Our results demonstrate that both thermal and mechanical hypersensitivity evoked by co-administration of BK and OLDA is mediated by the activation of spinal TRPV1 channels.
    WorkplaceInstitute of Physiology
    ContactLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Year of Publishing2022
    Electronic addresshttps://www.mdpi.com/1422-0067/22/7/3712
Number of the records: 1  

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