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Gastric reflexes involve stimulation of sensory vagal fibers, which engage brainstem circuits that modulate efferent output back to the stomach, thereby completing the vago\u2010vagal reflex. Our recent studies in a rodent model of experimental high thoracic (T3\u2010) <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> suggest that reduced vagal afferent sensitivity to gastrointestinal (<jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>) stimuli may be responsible for diminished gastric function. Nevertheless, derangements in efferent signals from the dorsal motor nucleus of the vagus (<jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content>) to the stomach may also account for reduced motility.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We assessed the anatomical, neurophysiological, and functional integrity of gastric\u2010projecting <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> neurons in T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> rats using: (i) retrograde labeling of gastric\u2010projecting <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> neurons; (ii) whole cell recordings from gastric\u2010projecting neurons of the <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content>; and, (iii) <jats:italic>in vivo<\/jats:italic> measurements of gastric contractions following unilateral microinjection of thyrotropin\u2010releasing hormone (<jats:styled-content style=\"fixed-case\">TRH<\/jats:styled-content>) into the <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Immunohistochemical analysis of gastric\u2010projecting <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> neurons demonstrated no difference between control and T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> rats. Whole cell <jats:italic>in vitro<\/jats:italic> recordings showed no alteration in <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> membrane properties and the neuronal morphology of these same, neurobiotin\u2010labeled, <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> neurons were unchanged after T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> with regard to cell size and dendritic arborization. Central microinjection of <jats:styled-content style=\"fixed-case\">TRH<\/jats:styled-content> induced a significant facilitation of gastric contractions in both control and T3\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> rats and there were no significant dose\u2010dependent differences between groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>Our data suggest that the acute, 3\u00a0day to 1\u00a0week post\u2010<jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>, dysfunction of vagally mediated gastric reflexes do not include derangements in the efferent <jats:styled-content style=\"fixed-case\">DMV<\/jats:styled-content> motoneurons.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.12452","type":"journal-article","created":{"date-parts":[[2014,10,15]],"date-time":"2014-10-15T08:41:57Z","timestamp":1413362517000},"page":"1717-1729","source":"Crossref","is-referenced-by-count":11,"title":["Gastric vagal motoneuron function is maintained following experimental spinal cord injury"],"prefix":"10.1111","volume":"26","author":[{"given":"E. 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