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Experimental spinal cord injury alters the dose response of vagal motoneurons to TRH
Author(s) -
Holmes Gregory M,
Swartz Emily M
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.701.8
Subject(s) - efferent , vagus nerve , dorsal motor nucleus , reflex , spinal cord , medicine , efferent neuron , neuroscience , microinjection , gastric emptying , spinal cord injury , motility , anesthesia , stomach , biology , afferent , stimulation , genetics
Spinal cord injury (SCI) elicits immediate and profound gastric dysmotility. The stomach is modulated by gastric sensory signals transmitted via the vagus nerve to the nucleus tractus solitarius (NTS). The NTS integrates sensory information with signals from throughout the CNS and projects to nuclei which include preganglionic efferent neurons located in the dorsal motor nucleus of the vagus (DMV). This vago‐vagal reflex remains anatomically intact after SCI and our previous reports suggest that SCI diminishes vagal afferent sensitivity. However, derangements in efferent signals to the stomach may also account for reduced motility. Thyrotropin releasing hormone (TRH) profoundly modulates gastric motility by a direct depolarization of DMV neurons and offers a pharmacological tool to test DMV efferent integrity. We tested the hypothesis that experimental SCI induces functional impairment of rat DMV motoneurons by microinjecting TRH into the DMV 3 days after SCI or control surgery. Our data reveal a rightward dose‐response shift to unilateral DMV microinjection of TRH (0, 3, 10, 30 or 100 pmoles, n=40 total). Specifically, gastric motility response to 3pmoles TRH was reduced in SCI animals vs. surgical controls. Combined with our previous reports, these data suggest that SCI may also impair vagal preganglionic motoneurons. The mechanism leading to this impairment remains to be determined.