COOPERATION BETWEEN NEURAL AND MYOGENIC MECHANISMS IN THE CONTROL OF DISTENSION-INDUCED PERISTALSIS IN THE MOUSE SMALL-INTESTINE

1. Myogenic and neural control of intestinal transit were investigated in a model of distension-induced peristalsis. A comparison was made b etween the electrical and mechanical activities and outflow of content s observed in control mice and in W/W-v mice, which lack the interstit ial cells of Cajal associated with Auerbach's plexus. 2. Distension ca used a periodic appearance of increased motor activity due to stimulat ion of enteric nerves in both control and W/W-v mice. Excitation was p rimarily delivered by cholinergic nerves, whereas periodic inhibition was mediated by neuronal nitric oxide. 3. In control mice, outflow was driven by propagating slow-wave activity and was only in the aboral d irection. Outflow only occurred when slow waves carried sufficient act ion potentials to cause phasic intraluminal pressure increases of grea ter than or equal to 1 cmH(2)O through direct stimulation of the muscu lature or by distension-induced neurally mediated activation. 4. In W/ W-v mice outflow was associated with propagating action potentials tha t occurred due to either neural stimulation or direct muscle stimulati on. Action potential propagation and outflow occurred in both oral and aboral directions. 5. In summary, in both control and W/W-v mice, dis tension induced periodic motor activity through stimulation of the ent eric nervous system. Intraluminal contents were not moved in front of such motor activity. Rather, within such periods of activity that occu rred concurrently throughout an entire segment, pulsatile outflow was directed by individual propagating slow waves with superimposed action potentials in control tissue, and by propagating action potentials in W/W-v mice, which lack interstitial cells of Cajal.