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Experimental spinal cord injury upregulates vagal nodose TRPV1 expression (902.4)
Author(s) -
Swartz Emily,
Deiter Gina,
Holmes Gregory
Publication year - 2014
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.28.1_supplement.902.4
Subject(s) - trpv1 , medicine , ischemia , anesthesia , nodose ganglion , vagus nerve , spinal cord , gastrointestinal tract , transient receptor potential channel , endocrinology , receptor , stimulation , psychiatry
The gastrointestinal (GI) tract is critically dependent upon adequate blood flow. Spinal cord injury (SCI) produces dramatic GI and vascular dysregulation, including vascular hypotension and, possibly, visceral hypoperfusion. We have previously shown that T3‐SCI in rats results in diminished visceral blood flow, increased expression of inflammatory markers and consequent gastrointestinal dysmotility. Vagal afferent injury has been shown to induce changes in cholecystokinin (CCK) and transient receptor potential vanilloid type 1 receptor (TRPV1) expression within the nodose ganglion. We hypothesized that SCI leads to increased activation of TRPV1 channels along the vagus nerve. Nodose ganglia TRPV1 and CCK mRNA was quantified using qRT‐PCR, at 1‐day, 3‐days, and 7‐days post‐SCI and control. We used a superior mesenteric artery (SMA) occlusion model to show a worst case scenario of ischemia‐reperfusion to the GI tract. Our data show a significant increase in nodose TRPV1 and CCK of SCI and SMA rats compared to controls. The increased TRPV1 indicates GI inflammation and the increased CCK suggests that CCK increases as per vagal afferent injury. Our data present similarities to experimental ischemia‐reperfusion of the GI tract, in which SMA occlusion causes a dramatic inflammatory response within the GI tract. We propose that our model of SCI represents a continuum of GI ischemia and that the increase in inflammatory mediators and TRPV1 activation may play a role in the post‐SCI pathophysiology of gastric vagal afferents. Grant Funding Source : Supported by: NINDS 49177