Activation of glial cells in the spinal cord of a model of lumbar radiculopathy.

PURPOSE

Glial cells in the spinal cord of a lumbar radiculopathy model were investigated using immunohistochemical methods. Neuropathic pain is a consequence of neural plasticity. In models of neuropathic pain models, roles for glial cells in the development of pain behaviors have been reported. Accumulating evidence suggests that activation of p38 mitogen-activated protein kinase (p38) in glial cells contributes to the pathogenesis of neuropathic pain. We examined whether activation of glial cells is involved in the development of neuropathic pain-like behavior observed in a model of lumbar radicular pain that we developed. However, the pathogenesis of lumbar radiculopathy and in particular the effect of spinal glial activation on pain transmission in the dorsal horn of the spinal cord are still not fully known.

METHODS

The left L5 spinal root of Sprague-Dawley rats was ligated proximal to the DRG to produce models of lumbar radiculopathy. Protein levels of phosphorylated-p38 (p-p38) in the spinal cord were quantified by Western blot analysis. Double-immunofluorescense studies of p-p38 and specific markers of glia and neurons were performed to determine when and which types of cells were activated in the spinal cord.

RESULTS

We observed p38 activation in hyperactive microglia in the dorsal horn ipsilateral to surgery at 1 and 7 days after root constriction, but not in astrocytes or neurons.

CONCLUSIONS

Constriction of the lumbar root activated microglia in the spinal cord at 1 and 7 days after surgery, and then returned to normal state at 28 days after surgery, while pain behavior continued. These findings suggest that development of lumbar radicular pain may be initiated by activation of microglia.