# Can Transcutaneous Vagus Nerve Stimulation be Effective After Rats’ Spinal Cord Injury?

**Authors:** Tomoko Tanaka, Murat Gokden, Reid D Landes

PMC · DOI: 10.7759/cureus.102944 · 2026-02-04

## TL;DR

This study explores whether transcutaneous vagus nerve stimulation can reduce inflammation after spinal cord injuries in rats, finding some promising but not statistically significant trends.

## Contribution

The study investigates the potential anti-inflammatory effects of transcutaneous vagus nerve stimulation in a rat model of spinal cord injury.

## Key findings

- t-VNS did not significantly alter macrophage distribution in SCI rats.
- Post-hoc analysis showed a faster decline in M1 macrophages over time in the t-VNS group.
- Results suggest a possible anti-inflammatory effect of t-VNS, though not statistically significant.

## Abstract

Introduction: Most spinal cord injuries (SCIs) result from trauma, and despite extensive research, no curative treatment exists. SCIs occur from primary and secondary injuries. The primary injury is caused by direct impact from the initial trauma, mechanical disruption, dislocation, stretch, compression, or ischemia involving the spinal cord. The primary injury leads to a secondary injury, characterized by the sequential progression of cell dysfunction and death, which begins with an influx of inflammatory cells and cytokines and ultimately results in apoptosis, necrosis, and gliosis. Thus, mitigating the neuroinflammatory process has been a key focus in treating further secondary injuries by multiple modalities, which include vagus nerve stimulation (VNS). The present project investigated the effect of transcutaneous VNS (t-VNS) on the inflammatory effects of SCI.

Methods: The histopathology of the SCI contusion model in male Sprague-Dawley rats was compared between groups that received t-VNS and those that did not.

Result: No statistical difference was found between SCI with and without t-VNS in M1, M2a, M2b, and M2c macrophages (all p>0.27). However, post-hoc correlations indicated M1 macrophages declined more rapidly over time in the t-VNS group. (Spearman r= -0.50; 95% CI: -0.78, -0.05).

Conclusions: Although t-VNS did not significantly alter macrophage distribution, trends toward reduced M1 activation suggest a possible anti-inflammatory effect in the desired direction.

## Linked entities

- **Diseases:** spinal cord injury (MONDO:0043797)

## Full-text entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Cd163 (CD163 molecule) [NCBI Gene 312701] {aka ED2}, Il10 (interleukin 10) [NCBI Gene 25325] {aka IL10X, If2a}, Arg1 (arginase 1) [NCBI Gene 29221], IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** injuries (MESH:D014947), VNS (MESH:D020421), inflammatory (MESH:D007249), hematoma (MESH:D006406), neurotoxic (MESH:D020258), weakness (MESH:D018908), neurogenic bladder (MESH:D001750), traumatic brain injury (MESH:D000070642), edema (MESH:D004487), neuroinflammatory (MESH:D000090862), cardiac arrhythmia (MESH:D001145), stroke (MESH:D020521), ischemia (MESH:D007511), vocal cord paralysis (MESH:D014826), SCI (MESH:D013119), swelling of the spinal cord (MESH:D013118), autonomic (MESH:D001342), epilepsy (MESH:D004827), gliosis (MESH:D005911), infection (MESH:D007239), cardiovascular disease (MESH:D002318), immune diseases (MESH:D007154), neurological and psychological diseases (MESH:D000067073), acute infarct (MESH:D056989), contusion (MESH:D003288), infarct (MESH:D007238), chronic pain (MESH:D059350), dislocation (MESH:D004204), migraines (MESH:D008881), necrosis (MESH:D009336)
- **Chemicals:** paraffin (MESH:D010232), t (MESH:D014316), isoflurane (MESH:D007530), SQ (-), H&amp;E (MESH:D006371), Hematoxylin (MESH:D006416), paraformaldehyde (MESH:C003043), iodine (MESH:D007455), buprenorphine (MESH:D002047), eosin (MESH:D004801), clodronate (MESH:D004002)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Rodentia (rodent, order) [taxon 9989], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12964494/full.md

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Source: https://tomesphere.com/paper/PMC12964494