ArticleNeurogastroenterology and motility2014
Gastric vagal motoneuron function is maintained following experimental spinal cord injury.
Article in Neurogastroenterology and motility, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Role of voltage-gated CaJournal of neurophysiology · 2025Article
- Dysfunction of pancreatic exocrine secretion after experimental spinal cord injury.Experimental neurology · 2025Article
- Feasibility Study of Bariatric Surgery in a Rat Model of Spinal Cord Injury to Achieve Beneficial Body Weight Outcome.Neurotrauma reports · 2022Article
- Altered physiology of gastrointestinal vagal afferents following neurotrauma.Neural regeneration research · 2021Review
- Neuro-Immune Modulation Effects of Sacral Nerve Stimulation for Visceral Hypersensitivity in Rats.Frontiers in neuroscience · 2021Article
- Diminished enteric neuromuscular transmission in the distal colon following experimental spinal cord injury.Experimental neurology · 2020Article
- CD8 T Cells and STAT1 Signaling Are Essential Codeterminants in Protection from Polyomavirus Encephalopathy.Journal of virology · 2020Article
- Gastric vagal afferent neuropathy following experimental spinal cord injury.Experimental neurology · 2020Article
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
- PD-1 Dynamically Regulates Inflammation and Development of Brain-Resident Memory CD8 T Cells During Persistent Viral Encephalitis.Frontiers in immunology · 2019Article
- Anatomical and Functional Changes to the Colonic Neuromuscular Compartment after Experimental Spinal Cord Injury.Journal of neurotrauma · 2018Article
- Diminished gastric prokinetic response to ghrelin in a rat model of spinal cord injury.Neurogastroenterology and motility · 2018Article
- Mesenteric vascular dysregulation and intestinal inflammation accompanies experimental spinal cord injury.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundClinical reports indicate that spinal cord injury (SCI) initiates profound gastric dysfunction. Gastric reflexes involve stimulation of sensory vagal fibers, which engage brainstem circuits that modulate efferent output back to the stomach, thereby completing the vago-vagal reflex. Our recent studies in a rodent model of experimental high thoracic (T3-) SCI suggest that reduced vagal afferent sensitivity to gastrointestinal (GI) stimuli may be responsible for diminished gastric function. Nevertheless, derangements in efferent signals from the dorsal motor nucleus of the vagus (DMV) to the stomach may also account for reduced motility.
methodsWe assessed the anatomical, neurophysiological, and functional integrity of gastric-projecting DMV neurons in T3-SCI rats using: (i) retrograde labeling of gastric-projecting DMV neurons; (ii) whole cell recordings from gastric-projecting neurons of the DMV; and, (iii) in vivo measurements of gastric contractions following unilateral microinjection of thyrotropin-releasing hormone (TRH) into the DMV. KEY
resultsImmunohistochemical analysis of gastric-projecting DMV neurons demonstrated no difference between control and T3-SCI rats. Whole cell in vitro recordings showed no alteration in DMV membrane properties and the neuronal morphology of these same, neurobiotin-labeled, DMV neurons were unchanged after T3-SCI with regard to cell size and dendritic arborization. Central microinjection of TRH induced a significant facilitation of gastric contractions in both control and T3-SCI rats and there were no significant dose-dependent differences between groups. CONCLUSIONS & INFERENCES: Our data suggest that the acute, 3 day to 1 week post-SCI, dysfunction of vagally mediated gastric reflexes do not include derangements in the efferent DMV motoneurons.
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