Abstract
Neuropathic pain is often a consequence of nerve injury or of diseases such as diabetes, HIV AIDS or cancer, that damage peripheral nerves. Neuropathic pain can be agonizing, persistent over long periods, and, unfortunately, is often resistant to known pain-killers. Recent advances in our understanding of the mechanisms producing neuropathic pain have been made by defining causal roles of spinal microglia in the pathogenesis of neuropathic pain. Within spinal dorsal horn, peripheral nerve injury leads to a progressive series of changes in microglia including morphological hypertrophy of cell body and proliferation taken as indicative of activation. Furthermore, several molecules including P2X4 receptors, which are present in activated microglia, have been found to be required molecular mediators. We expect that understanding the key roles of these molecules in spinal microglia may lead to new strategies for the management of neuropathic pain, strategies not previously anticipated by a neuron-centric view of pain plasticity in the dorsal horn.
