Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/101723
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dc.contributor.authorDodds, K.en
dc.contributor.authorBeckett, E.en
dc.contributor.authorEvans, S.en
dc.contributor.authorGrace, P.en
dc.contributor.authorWatkins, L.en
dc.contributor.authorHutchinson, M.en
dc.date.issued2016en
dc.identifier.citationTranslational Psychiatry, 2016; 6(9):e888-1-e888-13en
dc.identifier.issn2158-3188en
dc.identifier.issn2158-3188en
dc.identifier.urihttp://hdl.handle.net/2440/101723-
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.en
dc.description.statementofresponsibilityKN Dodds, EAH Beckett, SF Evans, PM Grace, LR Watkins, and MR Hutchinsonen
dc.language.isoenen
dc.publisherNatureen
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/en
dc.subjectSpinal Cord; Neuroglia; Neurons; Animals; Humans; Neurogenic Inflammation; Sex Factors; Neuroimmunomodulation; Female; Male; Chronic Pain; Visceral Painen
dc.titleGlial contributions to visceral pain : implications for disease etiology and the female predominance of persistent painen
dc.typeJournal articleen
dc.identifier.rmid0030055040en
dc.identifier.doi10.1038/tp.2016.168en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1054091en
dc.relation.granthttp://purl.org/au-research/grants/arc/DP110100297en
dc.identifier.pubid264664-
pubs.library.collectionMedicine publicationsen
pubs.library.teamDS07en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
Appears in Collections:Medicine publications

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