Gastric vagal motoneuron function is maintained following experimental spinal cord injury

Background: Clinical 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. Methods: We 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 Results: Immunohistochemical 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. Gastrointestinal function is diminished following spinal cord injury. Gastric neurocircuitry remains anatomically intact after SCI; however, our previous studies suggest that activation of the afferent vagus is compromised in the days to weeks after injury. The integrity of vagal efferent (dorsal motor nucleus of the vagus, DMN) modulation of gastric contractions remained unexplored in the SCI model. The established central effects of thyrotropin-releasing hormone, TRH) upon gastric contractions provide a pharmacological tool for testing vagal efferent function. The aim of the present report was to elucidate the anatomical, neurophysiological, and functional integrity of the DMN in a rodent model of SCI. Using in vivo and in vitro neuropharmacological techniques, this study demonstrates that, unlike afferent input to gastric vagal neurocircuitry, the DMN remains functionally intact in the 3 day to 1 week acute phase of SCI. Our data suggest that post-SCI reduction in gastric contractions during this time frame is likely a result of presynaptic changes in gastric neural circuitry.