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.

Facet joints are implicated as a major source of neck and low-back pain. Both cervical and lumbar facet syndromes have been described in the medical literature. Biomechanical studies have shown that lumbar and cervical facet-joint capsules can undergo high strains during spine-loading. Neuroanatomic studies have demonstrated free and encapsulated nerve endings in facet joints as well as nerves containing substance P and calcitonin gene-related peptide. Neurophysiologic studies have shown that facet-joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors, and silent nociceptors. Inflammation leads to decreased thresholds of nerve endings in facet capsules as well as elevated baseline discharge rates. Recent biomechanical studies suggest that rear-end motor-vehicle impacts give rise to excessive deformation of the capsules of lower cervical facet joints. Still unresolved is whether this stretch is sufficient to activate nociceptors in the joint capsule. To answer this question, recent studies indicate that low stretch levels activate proprioceptors in the facet-joint capsule. Excessive capsule stretch activates nociceptors, leads to prolonged neural afterdischarges, and can cause damage to the capsule and to axons in the capsule. In instances in which a whiplash event is severe enough to injure the joint capsule, facet capsule overstretch is a possible cause of persistent neck pain.

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