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

K. N. Dodds, E. A.H. Beckett, S. F. Evans, P. M. Grace, L. R. Watkins, M. R. Hutchinson

Research output: Contribution to journalReview articlepeer-review

24 Citations (Scopus)
9 Downloads (Pure)

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.

Original languageEnglish
Article numbere888
Number of pages13
JournalTranslational Psychiatry
Volume6
Issue number9
DOIs
Publication statusPublished - 13 Sep 2016
Externally publishedYes

Bibliographical note

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 the material 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/

Keywords

  • glia
  • neuroimmune
  • pain
  • Female
  • Sex factors
  • central sensitization

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