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Effects of interleukin-1 beta, interleukin-6, and tumor necrosis factor on sensitivity of dorsal root ganglion and peripheral receptive fields in rats



Effects of interleukin-1 beta, interleukin-6, and tumor necrosis factor on sensitivity of dorsal root ganglion and peripheral receptive fields in rats



European Spine Journal 15(10): 1529-1537



This study was designed to characterize the effects of low doses (0.5-5 ng) of pro-inflammatory cytokines, interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor (TNF), on the neural activity of dorsal root ganglion (DRG) in rats. The purpose of this study was to examine the effects of cytokines (IL-1beta, IL-6, and TNF) on the somatosensory neural response of DRG. The release of inflammatory cytokines by an injured disc may play a critical role in pain production at nerve endings, axons, and nerve cell bodies. Herniated disc tissue has been shown to release IL-1beta, IL-6, TNF, and other algesic chemicals. Their effects on nerve endings in disc and adjacent tissue may lead to low back pain and their effects on dorsal root axons and ganglia may lead to sciatica. Exposed lumbar DRGs were investigated by electrophysiologic techniques. Sham (mineral oil), control (carrier solution), or IL-1beta, IL-6, or TNF at doses of 0.5, 1, and 5 ng were applied over the DRG. Baseline discharge rates as well as mechanosensitivity of the DRG and peripheral receptive fields were evaluated over 30 min. Applications of IL-1beta at 1 ng resulted in an increase in the discharge rate, 5 ng resulted in an increased mechanosensitivity of the DRG in group II units. Similarly, after 1 ng TNF applications, group II units also showed an increase in mechanosensitivity of DRG and peripheral receptive fields. At low doses IL-1beta and TNF sensitization of receptive fields were observed. The responses observed in the group II units indicate that a sub-population of afferent units might have long-term effects modifying the sensory input to the central nervous system. This study provides added evidence to the role of cytokines in modulating afferent activity following inflammation.

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Accession: 048909760

Download citation: RISBibTeXText

PMID: 16474945

DOI: 10.1007/s00586-005-0058-8


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