ArticleNeurogastroenterology and motility2011
Experimental spinal cord injury in rats diminishes vagally-mediated gastric responses to cholecystokinin-8s.
Article in Neurogastroenterology and motility, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- Taste Changes in a Rat Model of Spinal Cord Injury: Impact of High-Fat Diet and Weight Loss Surgery.Nutrients · 2026Article
- Role of voltage-gated CaJournal of neurophysiology · 2025Article
- Dysfunction of pancreatic exocrine secretion after experimental spinal cord injury.Experimental neurology · 2025Article
- Plasticity of colonic enteric nervous system following spinal cord injury in male and female rats.Neurogastroenterology and motility · 2023Article
- Gut Microbiota-Brain Axis as a Potential Modulator of Psychological Stress after Spinal Cord Injury.Biomedicines · 2022Review
- Spinal cord injury-mediated changes in electrophysiological properties of rat gastric nodose ganglion neurons.Experimental neurology · 2022Article
- 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
- Diminished enteric neuromuscular transmission in the distal colon following experimental spinal cord injury.Experimental neurology · 2020Article
- Effect of Low Intensity Magnetic Field Stimulation on Calcium-Mediated Cytotoxicity After Mild Spinal Cord Contusion Injury in Rats.Annals of neurosciences · 2020Article
- Gastric vagal afferent neuropathy following experimental spinal cord injury.Experimental neurology · 2020Article
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
- 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
- Risk factors for the development of osteoporosis after spinal cord injury. A 12-month follow-up study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2015Observational
- Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity.The Journal of physiology · 2015Article
- Gastric vagal motoneuron function is maintained following experimental spinal cord injury.Neurogastroenterology and motility · 2014Article
- Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Comprehensive Physiology · 2014Review
- Fabrication and implantation of miniature dual-element strain gages for measuring in vivo gastrointestinal contractions in rodents.Journal of visualized experiments : JoVE · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWe have shown recently that our model of experimental high-thoracic spinal cord injury (T3-SCI) mirrors the gastrointestinal clinical presentation of neurotrauma patients, whereby T3-SCI animals show diminished gastric emptying and dysmotility. In this study we used cholecystokinin as a model peptide to test the hypothesis that the T3-SCI induced gastroparesis is due, in part, to an impaired vagally-mediated response to gastrointestinal peptides.
methodsWe measured the responses to sulfated cholecystokinin (CCK-8s) in control and T3-SCI (3 or 21 days after injury) rats utilizing: (i) c-fos expression in the nucleus tractus solitarius (NTS) following peripherally administered CCK-8s; (ii) in vivo gastric tone and motility following unilateral microinjection of CCK-8s into the dorsal vagal complex (DVC); and (iii) whole cell recordings of glutamatergic synaptic inputs to NTS neurons. KEY
resultsOur results show that: (i) medullary c-fos expression in response to peripheral CCK-8s was significantly lower in T3-SCI rats 3 days after the injury, but recovered to control values at 3 weeks post-SCI, (ii) Unilateral microinjection of CCK-8s in the DVC induced a profound gastric relaxation in control animals, but did not induce any response in T3-SCI rats at both 3 and 21 days after SCI, (iii) Perfusion with CCK-8s increased glutamatergic currents in 55% of NTS neurons from control rats, but failed to induce any response in NTS neurons from T3-SCI rats. CONCLUSIONS & INFERENCES: Our data indicate alterations of vagal responses to CCK-8s in T3-SCI rats that may reflect a generalized impairment of gastric vagal neurocircuitry, leading to a reduction of gastric functions after SCI.
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