Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/101723
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Glial contributions to visceral pain : implications for disease etiology and the female predominance of persistent pain
Author: Dodds, K.
Beckett, E.
Evans, S.
Grace, P.
Watkins, L.
Hutchinson, M.
Citation: Translational Psychiatry, 2016; 6(9):e888-1-e888-13
Publisher: Nature
Issue Date: 2016
ISSN: 2158-3188
2158-3188
Statement of
Responsibility: 
KN Dodds, EAH Beckett, SF Evans, PM Grace, LR Watkins, and MR Hutchinson
Abstract: In 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.
Keywords: Spinal Cord; Neuroglia; Neurons; Animals; Humans; Neurogenic Inflammation; Sex Factors; Neuroimmunomodulation; Female; Male; Chronic Pain; Visceral Pain
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/
RMID: 0030055040
DOI: 10.1038/tp.2016.168
Grant ID: http://purl.org/au-research/grants/nhmrc/1054091
http://purl.org/au-research/grants/arc/DP110100297
Appears in Collections:Medicine publications

Files in This Item:
File Description SizeFormat 
hdl_101723.pdfPublished version1.53 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.