2005•Unpublished venueRequires access
IMMUNOFLUORESCENCE STAINING FOR INFLAMMATION-RELATED MOLECULESIN THE DORSAL ROOT GANGLIA OF RAT EXPERIMENTAL MODELS OFPERIPHERAL NEUROPATHIC PAIN
Kateřina Pejchalová, Petr Dubový, Radim Jančálek, Ilona Klusáková, Ivana Hradilová Svíženská
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Abstract
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.