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The underlying mechanisms of neuropathic pain are poorly understood, and existing treatments are mostly ineffective. We recently demonstrated that antisense mediated “knock-down” of the sodium channel isoform, Na_V1.8, reverses neuropathic pain behavior after L5/L6 spinal nerve ligation (SNL), implicating a critical functional role of Na_V1.8 in the neuropathic state. Here we have investigated mechanisms through which Na_V1.8 contributes to the expression of experimental neuropathic pain. Na_V1.8 does not appear to contribute to neuropathic pain through an action in injured afferents because the channel is functionally downregulated in the cell bodies of injured neurons and does not redistribute to injured terminals. Although there was little change in Na_V1.8 protein or functional channels in the cell bodies of uninjured neurons in L4 ganglia, there was a striking increase in Na_V1.8 immunoreactivity along the …