Volume 7, Number 3 (Summer 2016 -- 2016)                   BCN 2016, 7(3): 231-240 | Back to browse issues page




DOI: 10.15412/J.BCN.03070308
PMID: 27563416
PMCID: PMC4981835

Cited 0 times in PubMed Central

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Gazerani S, Zaringhalam J, Manaheji H, Golabi S. The Role of C Fibers in Spinal Microglia Induction and Possible Relation with TRPV3 Expression During Chronic Inflammatory Arthritis in Rats. BCN. 2016; 7 (3) :231-240
URL: http://bcn.iums.ac.ir/article-1-650-en.html

1- PhD student Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- MD, PhD Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Research Center, Shahid Beheshti University of Medical Sciences
3- Associated Professor Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:  

Introduction: Stimulation of peptidergic fibers activates microglia in the dorsal horn. Microglia activation causes fractalkine (FKN) release, a neuron-glia signal, which enhances pain. The transient vanilloid receptor 1 (TRPV1) mediates the release of neuropeptides, which can subsequently activate glia. TRPV1 and TRPV2 are generally expressed on C and Aδ fibers, respectively. Expression of both proteins is upregulated during inflammation, but expression of TRPV3 after induction of inflammation is unclear.
Methods: Adult male Wistar rats were used in all experiments. Arthritis was induced in them by single subcutaneous injection of complete Freund’s adjuvant (CFA) in their right hindpaws. Resiniferatoxin (RTX) was used to eliminate peptidergic fibers. We examined the relation between FKN and TRPV3 expression by administration of anti-FKN antibody.
Results: Our study findings indicated that 1) spinal TRPV3 was mostly expressed on nonpeptidergic fibers, 2) expression of spinal TRPV3 increased following inflammation, 3) elimination of peptidergic fibers decreased spinal TRPV3 expression, 4) alteration of hyperalgesia was compatible with TRPV3 changes in RTX-treated rat, and 5) anti-FKN antibody reduced spinal TRPV3 expression.
Conclusion: It seems that the hyperalgesia variation during different phases of CFA-induced arthritis correlates with spinal TRPV3 expression variation on peptidergic fibers. Moreover, spinal microglial activation during CFA inflammation is involved in TRPV3 expression changes via FKN signaling.

Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2015/03/2 | Accepted: 2015/08/27 | Published: 2016/07/1

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