Abstract
The aim of this study was to determine whether trinitrobenzene sulfonic acid-induced colitis leads to alterations in enteric neuronal transmission in hamsters. We assessed the mechanical responses induced by the application of electrical field stimulation (EFS) in isolated segments of the distal colon. The EFS-induced relaxation and contraction were blocked by a nitric oxide synthase inhibitor and by the combination of antagonists for tachykinin NK1 and NK2 receptors and muscarinic acetylcholine receptors, respectively. The mechanical responses to EFS were attenuated in the inflamed colon at 7days and were recovered by 30days after inflammation treatment. In addition, we found that purinergic and opioidergic excitatory neural components are expressed following the resolution of colitis. These results suggest that colonic inflammation causes indiscriminate damage to enteric neurons but that neuronal components are restored and that new excitatory neural components, compensating for the contractile responses in smooth muscle after colitis, are expressed.
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