Co‐operation between neural and myogenic mechanisms in the control of distension‐induced peristalsis in the mouse small intestine

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Abstract
Myogenic and neural control of intestinal transit were investigated in a model of distension‐induced peristalsis. A comparison was made between the electrical and mechanical activities and outflow of contents observed in control mice and in W/W v mice, which lack the interstitial cells of Cajal associated with Auerbach's plexus. Distension caused a periodic appearance of increased motor activity due to stimulation of enteric nerves in both control and W/W v mice. Excitation was primarily delivered by cholinergic nerves, whereas periodic inhibition was mediated by neuronal nitric oxide. In control mice, outflow was driven by propagating slow‐wave activity and was only in the aboral direction. Outflow only occurred when slow waves carried sufficient action potentials to cause phasic intraluminal pressure increases of ≥ 1 cmH2O through direct stimulation of the musculature or by distension‐induced neurally mediated activation. In W/W v mice, outflow was associated with propagating action potentials that occurred due to either neural stimulation or direct muscle stimulation. Action potential propagation and outflow occurred in both oral and aboral directions. In summary, in both control and W/W v mice, distension induced periodic motor activity through stimulation of the enteric nervous system. Intraluminal contents were not moved in front of such motor activity. Rather, within such periods of activity that occurred 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.