IMMUNOFLUORESCENCE STAINING FOR INFLAMMATION-RELATED MOLECULES IN THE DORSAL ROOT GANGLIA OF RAT EXPERIMENTAL MODELS OF PERIPHERAL NEUROPATHIC PAIN
| Authors | |
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| Year of publication | 2005 |
| Type | Article in Proceedings |
| Conference | Fifth conference of the Czech neuroscience society |
| MU Faculty or unit | |
| Citation | |
| Field | Neurology, neurosurgery, neurosciences |
| Keywords | primary sensory neurons; cytokines; sciatic nerve ligation; IL1-beta; IL-6; TNF-alpha; TNFR; satellite cells |
| Description | Peripheral neuropathic pain is induced by an injury or disease of the peripheral nerves, and related with cellular and molecular changes in the peripheral nervous system, spinal cord and brain. The primary sensory neurons of the dorsal root ganglia (DRG) play a key role in neuropathic hypersensibility (1). Several lines of evidence suggest that pro- and anti-inflammatory cytokines are initiators of changes in the activity of DRG neurons (2). Peripheral neuropathic pain has been investigated using rat peripheral nerve injury models including unilateral sciatic and spinal nerve ligation. The experimental models were utilized for the study of immunofluorescence (IF) staining for IL1-beta, IL-6, TNF-alpha and TNFR1 in the rat DRG. Quantitative and qualitative IF changes in the DRG affected by unilateral nerve injury were compared with the contralateral ones removed from operated animals as well as naive rats. Ipsi- and contralateral DRG displayed increased IF for TNF-alpha and TNFR1 when compared with DRG of naive rats. The TNF-alpha IF was increased in both DRG neurons and their satellite glial cells, while enhanced IF for TNFR1 was observed only at the surface of satellite glial cells after various types of nerve injury. In addition, ipsilateral DRG exhibited an elevation of TNF-alpha immunoreactivity by invaded ED-1+ macrophages. The IL1-beta IF was increased in the DRG neurons following sciatic and spinal nerve constriction. A higher level of IF for IL-6 was observed in the DRG neurons and their satellite glial cells. The results suggest that changes in proinflammatory cytokines and their receptors belong to a highly complex response to nerve lesion inducing neuropathic pain. (1) Woolf C.J., Mannion R.J.: Lancet 353: 1959-1964, 1999. (2) Schafers M., Lee D.H., Brors D. et al.: J. Neurosci. 23:3028ĄV3038, 2003. The study was supported by grants 309/03/1199 and MSM0021622404. |
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