Neuron Glia Biology

Research Article

Satellite glial cells express IL-6 and corresponding signal-transducing receptors in the dorsal root ganglia of rat neuropathic pain model

Petr Dubovýa1 c1, Ilona Klusákováa1*, Ivana Svíženskáa1* and Václav Brázdaa1a2

a1 Department of Anatomy, Division of Neuroanatomy, Faculty of Medicine, Masaryk University, Brno, Czech Republic

a2 Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno, Czech Republic

Abstract

There is a growing body of evidence that cytokines contribute to both induction and maintenance of neuropathic pain derived from changes in dorsal root ganglia (DRG), including the activity of the primary sensory neurons and their satellite glial cells (SGC). We used immunofluorescence and in situ hybridization methods to provide evidence that chronic constriction injury (CCI) of the sciatic nerve induces synthesis of interleukin-6 (IL-6) in SGC, elevation of IL-6 receptor (IL-6R) and activation of signal transducer and activator of transcription 3 (STAT3) signalling. Unilateral CCI of the rat sciatic nerve induced mechanoallodynia and thermal hyperalgesia in ipsilateral hind paws, but contralateral paws exhibited only temporal changes of sensitivity. We demonstrated that IL-6 mRNA and protein, which were expressed at very low levels in naïve DRG, were bilaterally increased not only in L4-L5 DRG neurons but also in SGC activated by unilateral CCI. Besides IL-6, substantial increase of IL-6R and pSTAT3 expression occurred in SGC following CCI, however, IL-6R associated protein, gp130 levels did not change. The results may suggest that unilateral CCI of the sciatic nerve induces bilateral activation of SGC in L4-L5 DRG to transduce IL-6 signalling during neuroinflammation.

Correspondence:

c1 Correspondence should be addressed to: Petr Dubový, Department of Anatomy, Division of Neuroanatomy, Faculty of Medicine, Masaryk University, Kamenice 3, CZ-625 00 Brno Czech Republic, phone: +420-5-549493701 fax: +420-5-549491323 email: pdubovy@med.muni.cz

Footnotes

* These authors contributed equally to this work.