261. In Vivo Over-Expression of Fractalkine, a Putative Neuron-to-Glia Signal, To Characterize Underlying Mechanisms of Neuropathic Pain

Abstract

We have previously shown that fractalkine (FKN), the newest member of the chemokine family, plays an integral role in the initiation and maintenance of exaggerated pain states. Fractalkine is expressed on the external surface of sensory nerves and some dorsal spinal cord neurons. The receptor for FKN is found predominately on spinal cord microglia. Strong neuronal excitation induces the cleavage of the FKN chemokine domain forming a soluble signal that can act on nearby glia. Spinal cord microglia are important in diverse forms of enhanced pain states via the release of the pro-inflammatory cytokines, interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF).