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The colonic migrating motor complex (CMMC) is a major pattern of motility that is entirely generated and organized by the enteric nervous system. We have previously demonstrated that the Na v 1.9 channel underlies a tetrodotoxin-resistant sodium current which modulates the excitability of enteric neurons. The aim of this study was to observe the effect of loss of the Na v 1.9 channel in enteric neurons on mouse colonic motility  in vitro . The mechanical activity of the circular muscle was simultaneously recorded from three sites, namely, proximal, mid- and distal, along the whole colon of male, age-matched wild-type and Na v 1.9 null mice. Spontaneous CMMCs were observed in all preparations. The mean frequency of CMMCs was significantly higher in the Na v 1.9 null mice (one every 2.87 ± 0.1 min compared to one every 3.96 ± 0.23 min in the wild type). The mean duration of CMMCs was shorter and the mean area-under-contraction was larger in the Na v 1.9 null mice compared to the wild type. In addition, CMMCs propagated preferentially in an aboral direction in the Na v 1.9 null mice. Our study demonstrates that CMMCs do occur in mice lacking the Na v 1.9 channel, but their characteristics are significantly different from controls. Up to now, the Na v 1.9 channel was mainly associated with nociceptive neurons and involved in their hyperexcitability after inflammation. Our result shows for the first time a role for the Na v 1.9 channel in a complex colonic motor pattern.

The Nav1.9 channel regulates colonic motility in mice