Transcutaneous auricular vagus nerve stimulation attenuates neuroinflammation in a mouse model of traumatic brain injury

Transcutaneous auricular vagus nerve stimulation (VNS) activated the solitary tract nucleus and the dorsal motor nucleus of the vagus nerve as evidenced by a significant upregulation of the neuronal activation marker c-Fos, indicating vagus nerve activation. Transcutaneous auricular VNS treatment reduced the expression of pro-inflammatory microglial markers Tnf (1.69 ± 0.17 vs. 3.615 ± 0.86, p < 0.05) and Lcn2 (64.15 ± 14 vs. 337.7 ± 104.8, p < 0.01) in the ipsilateral injured cortex on PIDs 3 and 7, respectively. Transcutaneous auricular VNS also increased the expression of anti-inflammatory microglial marker Arg1 (55 ± 6.47 vs. 30.49 ± 3.94, p < 0.01) and astrocyte Gfap reactivity (8,582 ± 826 vs. 4,569 ± 554.3, p < 0.01) on PID 3.

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Publication Details

Journal
The Journal of Trauma: Injury, Infection, and Critical Care
Published
2025-12-17
DOI
https://doi.org/10.1097/ta.0000000000004849
Primary Topic
Vagus Nerve Stimulation Research
Type
article
Field-Weighted Citation Impact
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article

Transcutaneous auricular vagus nerve stimulation attenuates neuroinflammation in a mouse model of traumatic brain injury

William B. Fulton, Mahmoud G. El Baassiri, Daniel Scheese, Johannes W. Duess et al.
The Journal of Trauma: Injury, Infection, and Critical Care
Vagus Nerve Stimulation Research
article

Transcutaneous auricular vagus nerve stimulation attenuates neuroinflammation in a mouse model of traumatic brain injury

William B. Fulton, Mahmoud G. El Baassiri, Daniel Scheese, Johannes W. Duess, Chhinder P. Sodhi, Isam W. Nasr, David Joel Hackam, Gene Y. Fridman, Cody Tragesser, Leonard Lawandos
article en

Abstract

Transcutaneous auricular vagus nerve stimulation (VNS) activated the solitary tract nucleus and the dorsal motor nucleus of the vagus nerve as evidenced by a significant upregulation of the neuronal activation marker c-Fos, indicating vagus nerve activation. Transcutaneous auricular VNS treatment reduced the expression of pro-inflammatory microglial markers Tnf (1.69 ± 0.17 vs. 3.615 ± 0.86, p < 0.05) and Lcn2 (64.15 ± 14 vs. 337.7 ± 104.8, p < 0.01) in the ipsilateral injured cortex on PIDs 3 and 7, respectively. Transcutaneous auricular VNS also increased the expression of anti-inflammatory microglial marker Arg1 (55 ± 6.47 vs. 30.49 ± 3.94, p < 0.01) and astrocyte Gfap reactivity (8,582 ± 826 vs. 4,569 ± 554.3, p < 0.01) on PID 3.

The Journal of Trauma: Injury, Infection, and Critical Care
Johns Hopkins University (US), Johns Hopkins Medicine (US)
Openalex Percentile: Top 52%
Vagus Nerve Stimulation Research
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