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Establishment of a novel brainstem ischemic dysphagia model: single-cell sequencing reveals the molecular mechanisms
Yueqin Tian1, Qianqian Wang2, Jiahui Hu1
1Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, No. 600, Tianhe Road, Guangzhou, 510630, Guangdong, China.
Objective:
Previous animal models of post-stroke dysphagia (PSD) have limitations-these models are primarily induced by cortical strokes. Compared to cortical strokes, brainstem strokes are more likely to cause dysphagia, and the pathological mechanisms underlying dysphagia differ by focal infarction location. This study aimed to create a novel rat dysphagia model via brainstem ischemia (BSI) and explore modified pharyngeal electrical stimulation (mPES) therapy.
Methods:
Rat brainstem ischemia was induced by photochemical embolization, confirmed by MRI and pathology. Swallowing function was assessed using Videofluoroscopic Swallowing Study (VFSS), while motor and neurobehavioral changes were evaluated through behavioral tests. Post-mPES treatment, VFSS was conducted to evaluate the swallowing function and single-cell transcriptomics was performed to explore therapeutic mechanisms.
Results:
The BSI model showed stable dysphagia characteristics, with prolonged pharyngeal transit time, increased inter-swallowing interval and smaller bolus size area. mPES significantly improved these parameters. Behavioral tests revealed BSI caused anxiety-like behavior and worse motor performance in rats. Single-cell transcriptomics indicated mPES treatment involved multiple biological mechanisms, possibly exerting therapeutic effects by influencing oligodendrocyte differentiation and myelin, or synapse regeneration and repair.
Conclusion:
The novel BSI-induced dysphagia model exhibited stable swallowing function deficits. mPES effectively improved these deficiencies, with therapeutic mechanisms potentially associated with oligodendrocytes.
Insights
A new rat model of brainstem ischemia (BSI)-induced dysphagia shows stable swallowing deficits. Modified pharyngeal electrical stimulation (mPES) therapy effectively improved swallowing function, potentially through oligodendrocyte-related mechanisms.
Area of Science:
- Neuroscience
- Stroke Research
- Swallowing Disorders
Background:
- Existing animal models for post-stroke dysphagia (PSD) often use cortical strokes, which differ pathologically from brainstem strokes that more commonly cause dysphagia.
- The location of infarction in the brainstem significantly influences the underlying mechanisms of dysphagia.
Purpose of the Study:
- To develop a novel rat model of dysphagia induced by brainstem ischemia (BSI).
- To investigate the therapeutic potential of modified pharyngeal electrical stimulation (mPES) for BSI-induced dysphagia.
Main Methods:
- Brainstem ischemia (BSI) was induced in rats using photochemical embolization and confirmed via MRI and pathology.
- Swallowing function was assessed using Videofluoroscopic Swallowing Study (VFSS).
- Neurobehavioral and motor functions were evaluated, and single-cell transcriptomics analyzed post-mPES treatment.
Main Results:
- The BSI model demonstrated consistent dysphagia, characterized by prolonged pharyngeal transit time, increased inter-swallowing intervals, and reduced bolus size.
- mPES treatment significantly improved VFSS parameters and ameliorated anxiety-like behavior and motor deficits in BSI rats.
- Single-cell transcriptomics suggested mPES may work by influencing oligodendrocyte differentiation, myelin repair, or synapse regeneration.
Conclusions:
- A novel rat model of BSI-induced dysphagia reliably replicates swallowing deficits.
- Modified pharyngeal electrical stimulation (mPES) shows efficacy in treating BSI-induced dysphagia.
- The therapeutic mechanisms of mPES may involve oligodendrocyte-related pathways.
