A ganglionic intestino-intestinal reflex activated by acute noxious challenge.

To investigate noxious stimulation- responsive neural circuits that could influence the gut, we recorded from intestinally directed (efferent) nerve filaments dissected from mesenteric nerves close to the small intestine in anaesthetized rats. These exhibited baseline multiunit activity that was almost unaffected by vagotomy and reduced only slightly by cutting the splanchnic nerves. The activity was halved by hexamethonium treatment. When an adjacent gut segment received an intraluminal stimulus, 2,4,6-trinitrobenzenesulfonate (TNBS) in 30% ethanol, mesenteric efferent nerve activity increased for more than one hour. The increased activity was almost unaffected by bilateral vagotomy or splanchnic nerve section, indicating a lack of central nervous involvement, but it was 60% reduced by hexamethonium. Spike sorting discriminated efferent single and predominantly single unit spike trains that responded to TNBS, were unaffected by splachnectomy, but were silenced by hexamethonium. Following noxious stimulation of one segment, the adjacent segment showed no evidence of suppression of gut motility or vasoconstriction. We conclude that luminal application of a noxious stimulus to the small intestine activates an entirely peripheral, intestino-intestinal reflex pathway. This pathway involves enteric intestinofugal neurons that excite postganglionic sympathetic neurons via a nicotinic synapse. We suggest that the final sympathetic efferent neurons that respond to a tissue damaging stimulus are distinct from vasoconstrictor, secretomotor and motility inhibiting neurons.