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Final Program


Final Congress Guide

Therapeutics

1000 Section - Transcutaneous auricular vagus nerve stimulation promotes post-stroke functional recovery by suppressing microglia-mediated synaptic elimination via cholinergic system

Wednesday, May 20, 2026
6:00 PM - 7:30 PM PT

    Presenting Author/Autor expositor(s)

  • xo

    xiaorong ouyang, MD

    Ph.D. Candidate
    Shanghai YangZhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center)
    Shanghai, Shanghai, China (People's Republic)

    • Co-Author/Coautor(s)

  • wc

    wen cheng, MD

    Ph.D. Candidate
    Shanghai YangZhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center)
    Shanghai, Shanghai, China (People's Republic)

  • YP

    Yijun Pan, MD

    Ph.D. Candidate
    Yangzhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center)
    Shanghai, Shanghai, China (People's Republic)

    • Corresponding Author/Autor a quien dirigir la corr(s)

  • BY

    Bin Yu, MD

    Chief Physician
    Yangzhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center)
    Shanghai, Shanghai, China (People's Republic)

  • LJ

    Lingjing Jin, PhD

    president
    Yangzhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center)
    shanghai, Shanghai, China (People's Republic)

Objectives : Ischemic stroke is a major cause of disability globally. Microglia play a key role in post-stroke neurological deficits. Transcutaneous auricular vagus nerve stimulation (taVNS) has been shown to activate cholinergic pathway to inhibit microglia-mediated neuroinflammation and promote post-stroke functional recovery, yet its effects on other microglial functions remain unclear. This study investigates whether taVNS activates the cholinergic system to inhibit microglia-mediated synaptic elimination, improving stroke prognosis.

Design: Photothrombotic stroke was induced in WT and ChAT-cre mice. taVNS was applied within one hour after modeling, once daily for 30 minutes over seven days. RNA-seq and c-Fos staining were used to identify related pathways. Inhibitory viruses AAV-EF1a-DIO-hM4Di-EGFP were injected into the basal forebrain of  ChAT-cre mice to suppress cholinergic neurons. Magnetic resonance imaging and TTC staining assessed infarct volume, while cylinder test, grid walking test, and ladder rung walking tests evaluated function. Immunofluorescence staining assessed microglia-mediated synaptic pruning in the peri-infarct cortex.

Results:

taVNS reduced infarct volume and ameliorated neurological deficits in PT mice. TTC and MRI showed that taVNS significantly decreased infarct size versus controls (p < 0.05). Functional assessments like cylinder, grid walking and ladder walking tests were all markedly improved after taVNS (p < 0.05). Mechanistically, taVNS suppressed microglial over-activation (CD68/Iba-1↓) and synaptic pruning (lysosome–PSD95 colocalization↓) in peri-infarct cortex (p < 0.05). RNA-seq and c-Fos showed taVNS up-regulated the cholinergic system and activated basal forebrain cholinergic neurons (p < 0.05). Chemogenetic inhibition of these neurons reversed taVNS-induced reductions in infarct size and functional improvements, restoring microglial activation and synaptic colocalization to control levels (p < 0.05).

Conclusion:

This study reveals that taVNS improves post-stroke neurological deficits by activating cholinergic neurons to suppress microglial synaptic pruning. The finding extends the cholinergic anti-inflammatory pathway into the framework of “synaptic homeostasis regulation” and positioning non-invasive vagus stimulation as a clinically ready, cholinergic-targeted stroke-rehabilitation modality.