Abstract
Neuropathic pain represents a significant and mounting burden on patients and society at large. Management of neuropathic pain, however, is both intricate and challenging, exacerbated by the limited quantity and quality of clinically available treatments. On this stage, dysfunctional voltage-gated ion channels, especially the presynaptic N-type voltage-gated calcium channel (VGCC) (Cav2.2) and the tetrodotoxin-sensitive voltage-gated sodium channel (VGSC) (Nav1.7), underlie the pathophysiology of neuropathic pain and serve as high profile therapeutic targets. Indirect regulation of these channels holds promise for the treatment of neuropathic pain. In this review, we focus on collapsin response mediator protein 2 (CRMP2), a protein with emergent roles in voltage-gated ion channel trafficking and discuss the therapeutic potential of targetting this protein.
Highlights
Pain is universal and ravages effects across the globe without discriminating by age or gender [1]
We focus on collapsin response mediator protein 2 (CRMP2) as a novel therapeutic target uniquely positioned to combat pain via regulation of voltage-gated ion channels
Dysfunction and dysregulation of voltage-gated sodium channels (VGSCs) – namely increased sodium channel activity, current density, and negatively shifted half maximal activation voltage – contribute to reduced thresholds for action potential initiation and heightened spike firing underlying the pathophysiology of pain [6]
Summary
Management of neuropathic pain, is both intricate and challenging, exacerbated by the limited quantity and quality of clinically available treatments. On this stage, dysfunctional voltage-gated ion channels, especially the presynaptic N-type voltage-gated calcium channel (VGCC) (Cav2.2) and the tetrodotoxin-sensitive voltage-gated sodium channel (VGSC) (Nav1.7), underlie the pathophysiology of neuropathic pain and serve as high profile therapeutic targets. Dysfunctional voltage-gated ion channels, especially the presynaptic N-type voltage-gated calcium channel (VGCC) (Cav2.2) and the tetrodotoxin-sensitive voltage-gated sodium channel (VGSC) (Nav1.7), underlie the pathophysiology of neuropathic pain and serve as high profile therapeutic targets Indirect regulation of these channels holds promise for the treatment of neuropathic pain.
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