Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain
Abstract
Chronic pain is maintained by persistent, maladaptive molecular processes, many of which converge on ion channels. In sensory neurons, these processes include transcriptional reprogramming, altered trafficking, and remodeling of the channel complexes that set membrane excitability. Accumulating evidence indicates that the major ion channel changes driving chronification of neuropathic pain are not restricted to injured sensory neurons but also arise within the adjacent population of spared neurons. Here we review the ion channel alterations that sustain chronic pain states, the mechanisms by which neurons modulate expression of these channels, and the electrophysiological and functional consequences of these shifts in expression profile. We close by examining existing therapeutics directed at these channels and their regulatory mechanisms, which may offer means of interrupting the maintenance of neuropathic pain.
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