CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain

Author:

Chew Lindsey A.1,Khanna Rajesh1234

Affiliation:

1. Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, U.S.A.

2. Department of Anesthesiology, College of Medicine, University of Arizona, Tucson, AZ 85724, U.S.A.

3. Department of Neuroscience Graduate Interdisciplinary Program, College of Medicine, University of Arizona, Tucson, AZ 85724, U.S.A.

4. The Center for Innovation in Brain Sciences, The University of Arizona Health Sciences, Tucson, AZ, U.S.A.

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.

Publisher

Portland Press Ltd.

Subject

General Medicine

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