Transcriptomics of the L5-Dorsal Root Ganglion After Spinal Cord Stimulation in the Rat Spared Nerve Injury Model

Samantha Wilcox, Illinois Wesleyan University

Abstract

Spinal cord stimulation (SCS) is an effective pain management therapy used to reduce chronic, neuropathic pain for individuals with whom traditional methods, particularly opioid use, have not been completely successful. SCS provides neural stimulation via an electrode array attached to the dorsal section of the spinal cord. The electrode emits an oscillating electric field that disrupts action potentials decreasing pain responses. Following neural damage, the production of inflammatory cytokines and other related proteins increase. SCS reverses many of these changes particularly in the dorsal root ganglion. However, the exact mechanism by which this process decreases pain on a biochemical level is not completely understood. The transcriptome, the range of mRNA expression, is a way to study the subsequent protein expression in an individual. Therefore, an examination of the transcriptome following nerve injury and subsequent SCS provides insight into the influence of these processes on gene expression. The present study was able to examine the changes to the transcriptome and identify changes in gene expression following the establishment of a chronic pain state and again following treatment with SCS. The study found that more unique changes to the transcriptome were at earlier stages of the pain model potentially indicating a different underlying mechanism in the acute stages compared to chronic stages of pain. Secondly, the study identified that at all stages of the pain model, treatment with SCS is associated with changes in gene expression related to the biological processes of humoral immune response, and (positive) regulation of cell population proliferation. Additionally, the study identified that in the chronic stages of the pain model, biological processes most commonly altered by SCS include immune response, inflammation, and cell activation and signaling.