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| Resource type: Journal Article DOI: 10.3389/fnmol.2018.00398 ID no. (ISBN etc.): 1662-5099 BibTeX citation key: GonzalezHernandez2018 View all bibliographic details |
Categories: , BioAcyl Corp Subcategories: , Oxytocin analgesia Creators: Charlet, Gonzalez-Hernandez Collection: Frontiers in Molecular Neuroscience |
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| Abstract |
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The hypothalamic non-apeptide oxytocin (OT) has several physiological functions, ranging from lactation to social attachment (Gimpl and Fahrenholz, 2001). More recently, a collection of evidence revealed that OT inhibits pain transmission at peripheral (Juif et al., 2013; de Araujo et al., 2014; Tzabazis et al., 2016; González-Hernández et al., 2017), spinal, and supraspinal levels (Eliava et al., 2016; Poisbeau et al., 2018). These data support the prospect that spinal OT could be translated into clinical pain practice (Rash et al., 2014; Eisenach et al., 2015; Condés-Lara et al., 2016). While the receptor(s) and intracellular mechanisms responsible for the OT-induced analgesia are under scrutiny, the main dogma relies on the activation of the OT receptor (OTR).
Oxytocin and spinal and peripheral analgesia. This schema depicts the proposed mechanism for the oxytocin-mediated peripheral analgesia. Oxytocin could act via either OTR and/or TRPV1 through a three-way path: (i) spinal cord central release, to inhibit WDR neuron activity either directly or via activation of GABAergic neurons; (ii) blood release, through pituitary, to inhibit either the cell body or peripheral nociceptive fibers of DRG neurons; and (iii) skin release, to directly inhibit the excitation of nociceptive fibers. WDR: wide-dynamic-range; DRG: dorsal root ganglia. Adapted from Grinevich and Charlet (2017). Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |