Abstract
Our understanding of human colonic motility, and autonomic reflexes that generate motor patterns, has increased markedly through high-resolution manometry. Details of the motor patterns are emerging related to frequency and propagation characteristics that allow linkage to interstitial cells of Cajal (ICC) networks. In studies on colonic motor dysfunction requiring surgery, ICC are almost always abnormal or significantly reduced. However, there are still gaps in our knowledge about the role of ICC in the control of colonic motility and there is little understanding of a mechanistic link between ICC abnormalities and colonic motor dysfunction. This review will outline the various ICC networks in the human colon and their proven and likely associations with the enteric and extrinsic autonomic nervous systems. Based on our extensive knowledge of the role of ICC in the control of gastrointestinal motility of animal models and the human stomach and small intestine, we propose how ICC networks are underlying the motor patterns of the human colon. The role of ICC will be reviewed in the autonomic neural reflexes that evoke essential motor patterns for transit and defecation. Mechanisms underlying ICC injury, maintenance, and repair will be discussed. Hypotheses are formulated as to how ICC dysfunction can lead to motor abnormalities in slow transit constipation, chronic idiopathic pseudo-obstruction, Hirschsprung's disease, fecal incontinence, diverticular disease, and inflammatory conditions. Recent studies on ICC repair after injury hold promise for future therapies.
Highlights
The colonic musculature is a super network of excitable cells, foremost the smooth muscle cells that do all the work, all the accessory cells that orchestrate contractions into functional patterns
As envisioned by Ramon y Cajal, the primary control systems are the interstitial cells of Cajal (ICC) and the intrinsic and extrinsic nervous systems that are intertwined and embedded in the musculature, such that little activity happens without the involvement of ICC or nerves
ICC generate slow-wave activity that is transmitted to the smooth musculature via gap junctions where they trigger slow-wave activity within smooth muscle cells, which actively propagates throughout the muscle layers [43]. Based on these animal studies, we reviewed in 1997 the possible role of ICC in human colon motor disorders and their potential role in treatment [44]
Summary
The colonic musculature is a super network of excitable cells, foremost the smooth muscle cells that do all the work, all the accessory cells that orchestrate contractions into functional patterns. The waning excitation following the HAPW generates a $12 cycles/min cyclic motor pattern This is very similar to the human MMC in the stomach in vivo, neural excitation evoking slow-wave-driven peristaltic activity. Similar to the human colon, the colonic motor complex in mice, likely the functional equivalent of the HAPW not identical in underlying mechanism, shows its rhythmic propulsive motor pattern to be dependent on neurally induced slow-wave pacemaker activity in ICC-MP [69, 71, 82]. A cyclic motor pattern within a single haustrum is a common observation during HRCM, as is the rhythmic activity of the sphincter-like circular musculature that bounds each haustrum, all at a dominant frequency of $3 cycles/min; associated with slow-wave activity of the ICC-SMP. The extent of ICC injury was not associated with the duration of the disease [178]; ICC injury and recovery may be a continuous process in chronic inflammation
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