ArticleNeurogastroenterology and motility2018
Diminished gastric prokinetic response to ghrelin in a rat model of spinal cord injury.
Article in Neurogastroenterology and motility, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Role of voltage-gated CaJournal of neurophysiology · 2025Article
- Dysfunction of pancreatic exocrine secretion after experimental spinal cord injury.Experimental neurology · 2025Article
- Editorial: Neuroendocrine research in health and disease, volume II.Frontiers in neuroscience · 2023Article
- The controversial role of the vagus nerve in mediating ghrelin's actions: gut feelings and beyond.IBRO neuroscience reports · 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
- Ghrelin-Mediated Regeneration and Plasticity After Nervous System Injury.Frontiers in cell and developmental biology · 2021Review
- Gastric vagal afferent neuropathy following experimental spinal cord injury.Experimental neurology · 2020Article
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPatients with cervical or high-thoracic spinal cord injury (SCI) often present reduced gastric emptying and early satiety. Ghrelin provokes motility via gastric vagal neurocircuitry and ghrelin receptor agonists offer a therapeutic option for gastroparesis. We have previously shown that experimental high-thoracic injury (T3-SCI) diminishes sensitivity to another gastrointestinal peptide, cholecystokinin. This study tests the hypothesis that T3-SCI impairs the vagally mediated response to ghrelin.
methodsWe investigated ghrelin sensitivity in control and T3-SCI rats at 3-days or 3-weeks after injury utilizing: (i) acute (3-day post-injury) fasting and post-prandial serum levels of ghrelin; (ii) in vivo gastric reflex recording following intravenous or central brainstem ghrelin; and (iii) in vitro whole cell recording of neurons within the dorsal motor nucleus of the vagus (DMV). KEY
resultsThe 2-day food intake of T3-SCI rats was reduced while fasting serum ghrelin levels were higher than in controls. Intravenous and fourth ventricle ghrelin increased in vivo gastric motility in fasted 3-day control rats but not fasted T3-SCI rats. In vitro recording of DMV neurons from 3-day T3-SCI rats were insensitive to exogenous ghrelin. For each measure, vagal responses returned after 3-weeks. CONCLUSIONS AND INFERENCES: Hypophagia accompanying T3-SCI produces a significant and physiologically appropriate elevation in serum ghrelin levels. However, higher ghrelin levels did not translate into increased gastric motility in the acute stage of T3-SCI. We propose that this may reflect diminished sensitivity of peripheral vagal afferents to ghrelin or a reduction in the responsiveness of medullary gastric vagal neurocircuitry following T3-SCI.
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