Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain
- 1Department of Biomedical Sciences, Texas A&M University, Dallas, TX 75246, USA
- 2Department of Pharmacology & Therapeutics, University of Florida, Gainesville, FL 32603, USA
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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BibTeX
@article{speidell2026spared,
title = {{Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain}},
author = {Andrew Speidell and Rajesh Khanna and Kimberly Gomez},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27188365},
url = {https://www.mdpi.com/1422-0067/27/18/8365},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain
AU - Andrew Speidell
AU - Rajesh Khanna
AU - Kimberly Gomez
PY - 2026
DA - 2026/09/19
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27188365
UR - https://www.mdpi.com/1422-0067/27/18/8365
AB - 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.
SN - 1422-0067
ER -