Activation of Microglial Cells: the Bridge between the Immune System and Pain in Central Nervous System
Journal of Cellular & Molecular Anesthesia,
Vol. 1 No. 4 (2016),
26 August 2016
,
Page 135-136
https://doi.org/10.22037/jcma.v1i4.13620
Abstract
Background: Pain is one of the main protests of inflammatory diseases, hence, understanding the mechanisms which involved in the induction and persistence of pain is essential. Microglia is a contributing factor in the onset and maintenance of inflammation. Increased microglial activation increases the level of central pro-inflammatory cytokines and the development of central sensitization following inflammation. The aim of this study was evaluate the relation of spinal microglia activity with pain related behaviors during Complete Freund’s adjuvant (CFA)-induced inflammation.
Materials and Methods: Inflammation caused by subcutaneous injection of Complete Freund’s adjuvant (CFA) in a single dose to the animals right hind paw. The edema and hyperalgesia caused by inflammation, respectively are measured by Plethysmometer and Radiant Heat, on days 0,7,14 and 21. Spinal Iba-1 protein expression was detected by Western blotting. Minocycline hydrochloride (Sigma, U.S.A) was administered i.p. at a dose of 40mg/kg daily.
Results: Our study findings indicated that CFA injection to right hindpaw of rats increased paw volume and hyperalgesia significantly during different stages of study, while Minocycline treatment significantly reduced paw volume and hyperalgesia. CFA injection into the right hindpaw of the rat increases the expression of molecules Ionized calcium binding adaptor molecule -1 (Iba-1) on different days of study, while Minocycline administration reduced spinal Iba-1 expression significantly compared to the CFA group.
Conclusion: The results of this study indicated the significant roles of microglia activation in deterioration of pain related behaviors during different stages of CFA-induced inflammation. The steady injection of Minocycline (as a microglia inhibitor) could reduce the inflammatory symptoms.
- pain
- microglia
- immune system
How to Cite
References
Suter MR. Microglial role in the development of chronic pain. Curr Opin Anaesthesiol. 2016;29(5):584-9.
Gomez Perdiguero E, Klapproth K, Schulz C, Busch K, Azzoni E, Crozet L, et al. Tissue-resident macrophages originate from yolk-sac-derived erythro-myeloid progenitors. Nature. 2015;518(7540):547-51.
Nasseri B NV, Manaheji H, Mousavi Z, Zaringhalam. Microglia are involved in pain related behaviors during the acute and chronic phases of arthritis inflammation. J Cell Mol Anesth. 2016;1(4):137-45.
Matsumura Y, Yamashita T, Sasaki A, Nakata E, Kohno K, Masuda T, et al. A novel P2X4 receptor-selective antagonist produces anti-allodynic effect in a mouse model of herpetic pain. Scientific reports. 2016;6:32461.
Volonte C, Apolloni S, Skaper SD, Burnstock G. P2X7 receptors: channels, pores and more. CNS Neurol Disord Drug Targets. 2012;11(6):705-21.
Tsuda M. Microglia in the spinal cord and neuropathic pain. Journal of diabetes investigation. 2016;7(1):17-26.
Kuan YH, Shyu BC. Nociceptive transmission and modulation via P2X receptors in central pain syndrome. Molecular brain. 2016;9(1):58.
Barbera-Cremades M, Baroja-Mazo A, Gomez AI, Machado F, Di Virgilio F, Pelegrin P. P2X7 receptor-stimulation causes fever via PGE2 and IL-1beta release. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2012;26(7):2951-62.
Bartlett R, Yerbury JJ, Sluyter R. P2X7 receptor activation induces reactive oxygen species formation and cell death in murine EOC13 microglia. Mediators Inflamm. 2013;2013:271813.
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