European journal of pain : EJP
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Peripheral nerve injury resulting in neuropathic pain induces the upregulation of interleukin (IL)-6 and tumor necrosis factor-alpha, which binds to tumor necrosis factor receptor 1 (TNFR1) and induces NF-kappaB and p38 MAPK activation in the spinal cord and dorsal root ganglia (DRG). We here investigated whether TNFR1 regulates IL-6 expression through NF-kappaB or p38 MAPK activations in the spinal cord and DRG in rats with chronic constriction injury (CCI) of the sciatic nerve. ⋯ In addition, NF-kappaB decoy, but not p38 MAPK inhibitor, SB203580 reduced CCI-elevated IL-6 expression in the spinal cord and DRG. Therefore, these data suggest that TNFR1 induces IL-6 upregulation and neuropathic pain through NF-kappaB, but not p38 MAPK activation in the spinal cord and DRG and that the NF-kappaB/IL-6 pathways in the DRG may be less dependent on TNFR1 than the spinal cord pathway.
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High pain threshold is a supportive diagnosis criterion for Prader-Willi syndrome (PWS), but its pathogenesis is poorly understood. In this study we investigate sensory pathways in PWS, in order to evaluate peripheral or central involvement in altered sensory perception. ⋯ Our data suggest that altered perception in PWS does not seem attributable to a peripheral nerve derangement due to metabolic factors or obesity. Impairment of the small nociceptive neurons of dorsal root ganglia or involvement of hypothalamic region may not be excluded.