UPREGULATION OF IL-6 AND ITS SIGNALING MOLECULES IN THE DORSAL ROOT GANGLIA OF LUMBAR AND CERVICAL SEGMENTS AND THEIR INVOLVEMENT IN NEUROPATHIC PAIN INDUCTION
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|Background and aims. Interleukin-6 (IL-6) is a key component of the nervous system response to an injury with various effects. The aim of the present study was to investigate alterations of IL-6 and its signaling in both ipsilateral and contralateral L4-L5 as well as C7-C8 dorsal root ganglia (DRG) in rat neuropathic pain models. Methods. Unilateral chronic constriction (CCI) and spared nerve injury (SNI) of the sciatic nerve was performed aseptically in sixty rats. Neuropathic pain induction was tested by measurement of mechanoallodynia and thermal hyperalgesia. Expression of IL-6, IL-6R, gp130, STAT-3 and SOCS3 was investigated bilaterally in lumbar (L4-5) and cervical (C7-8) DRG 1, 3, 7 and 14 days after surgery. Some DRG sections were simultaneously immunostained for GAP-43. To prove a pathway for neuroinflammatory propagation, FluoroRuby was injected intrathecally at the level of L4-L5 spinal segments in six CCI-operated rats. Results. Ipsilateral hind paws of all rats operated on CCI/SNI displayed mechanoallodynia and thermal hyperalgesia while contralateral hind paws and forepaws of both sides exhibited no significant hypersensitivity. Bilateral elevation of IL-6 and its signal molecules was not limited to lumbar, but also extended to cervical DRG. FluoroRuby applied intrathecally diffused into both lumbar and cervical DRG. Conclusions. The results suggest that up-regulation of IL-6 and its signaling is not only associated with neuropathic pain induction. Neuroinflammatory reaction to neuropathic stress is propagated alongside neuroaxis from lumbar to remote DRG related probably with conditioning of the cervical DRG neurons to injury.