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Ghrelin provokes motility via gastric vagal neurocircuitry and ghrelin receptor agonists offer a therapeutic option for gastroparesis. We have previously shown that experimental high\u2010thoracic injury (T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>) diminishes sensitivity to another gastrointestinal peptide, cholecystokinin. This study tests the hypothesis that T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>impairs the vagally mediated response to ghrelin.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We investigated ghrelin sensitivity in control and T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>rats at 3\u2010days or 3\u2010weeks after injury utilizing: (i) acute (3\u2010day post\u2010injury) fasting and post\u2010prandial 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 (<jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>The 2\u2010day food intake of T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>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\u2010day control rats but not fasted T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>rats. In vitro recording of<jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content>neurons from 3\u2010day T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>rats were insensitive to exogenous ghrelin. For each measure, vagal responses returned after 3\u2010weeks.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Inferences<\/jats:title><jats:p>Hypophagia accompanying T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>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\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>. 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\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.13258","type":"journal-article","created":{"date-parts":[[2017,12,5]],"date-time":"2017-12-05T12:01:52Z","timestamp":1512475312000},"source":"Crossref","is-referenced-by-count":11,"title":["Diminished gastric prokinetic response to ghrelin in a rat model of spinal cord injury"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6641-8280","authenticated-orcid":false,"given":"E. 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