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Glial contributions to visceral pain : implications for disease etiology and the female predominance of persistent pain

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dc.contributor.authorDodds, K.
dc.contributor.authorBeckett, E.
dc.contributor.authorEvans, S.
dc.contributor.authorGrace, P.
dc.contributor.authorWatkins, L.
dc.contributor.authorHutchinson, M.
dc.date.issued2016
dc.description.abstractIn the central nervous system, bidirectional signaling between glial cells and neurons ('neuroimmune communication') facilitates the development of persistent pain. Spinal glia can contribute to heightened pain states by a prolonged release of neurokine signals that sensitize adjacent centrally projecting neurons. Although many persistent pain conditions are disproportionately common in females, whether specific neuroimmune mechanisms lead to this increased susceptibility remains unclear. This review summarizes the major known contributions of glia and neuroimmune interactions in pain, which has been determined principally in male rodents and in the context of somatic pain conditions. It is then postulated that studying neuroimmune interactions involved in pain attributed to visceral diseases common to females may offer a more suitable avenue for investigating unique mechanisms involved in female pain. Further, we discuss the potential for primed spinal glia and subsequent neurogenic inflammation as a contributing factor in the development of peripheral inflammation, therefore, representing a predisposing factor for females in developing a high percentage of such persistent pain conditions.
dc.description.statementofresponsibilityKN Dodds, EAH Beckett, SF Evans, PM Grace, LR Watkins, and MR Hutchinson
dc.identifier.citationTranslational Psychiatry, 2016; 6(9):e888-1-e888-13
dc.identifier.doi10.1038/tp.2016.168
dc.identifier.issn2158-3188
dc.identifier.issn2158-3188
dc.identifier.orcidDodds, K. [0000-0003-0555-868X]
dc.identifier.orcidBeckett, E. [0000-0001-8256-0375]
dc.identifier.orcidEvans, S. [0000-0003-0347-604X]
dc.identifier.orcidGrace, P. [0000-0002-8999-1220]
dc.identifier.orcidHutchinson, M. [0000-0003-2154-5950]
dc.identifier.urihttp://hdl.handle.net/2440/101723
dc.language.isoen
dc.publisherNature
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1054091
dc.relation.granthttp://purl.org/au-research/grants/arc/DP110100297
dc.rights© The Author(s) 2016. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if thematerial is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/ by/4.0/
dc.source.urihttps://doi.org/10.1038/tp.2016.168
dc.subjectSpinal Cord
dc.subjectNeuroglia
dc.subjectNeurons
dc.subjectAnimals
dc.subjectHumans
dc.subjectNeurogenic Inflammation
dc.subjectSex Factors
dc.subjectNeuroimmunomodulation
dc.subjectFemale
dc.subjectMale
dc.subjectChronic Pain
dc.subjectVisceral Pain
dc.titleGlial contributions to visceral pain : implications for disease etiology and the female predominance of persistent pain
dc.typeJournal article
pubs.publication-statusPublished

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