Abstract
Normal motility of the colon is critical for quality of life and efforts to normalize abnormal colon function have had limited success. A better understanding of control systems of colonic motility is therefore essential. We report here a hypothesis with supporting experimental data to explain the origin of rhythmic propulsive colonic motor activity induced by general distention. The theory holds that both networks of interstitial cells of Cajal (ICC), those associated with the submuscular plexus (ICC–SMP) and those associated with the myenteric plexus (ICC–MP), orchestrate propagating contractions as pacemaker cells in concert with the enteric nervous system (ENS). ICC–SMP generate an omnipresent slow wave activity that causes propagating but non-propulsive contractions (“rhythmic propagating ripples”) enhancing absorption. The ICC–MP generate stimulus-dependent cyclic depolarizations propagating anally and directing propulsive activity (“rhythmic propulsive motor complexes”). The ENS is not essential for both rhythmic motor patterns since distention and pharmacological means can produce the motor patterns after blocking neural activity, but it supplies the primary stimulus in vivo. Supporting data come from studies on segments of the rat colon, simultaneously measuring motility through spatiotemporal mapping of video recordings, intraluminal pressure, and outflow measurements.
Highlights
Our understanding of colon motility, dysmotility, and potential treatments is still in its infancy
We propose that there are two independent pacemakers in the rat colon, one housed in the interstitial cells of Cajal (ICC)–SMP that is independent of the enteric nervous system (ENS) and the other housed in the ICC–MP that is stimulus-dependent, usually dependent on neural activity in vivo
The first pattern consisted of rhythmic, low frequency (0.3–2/min; average 1.2 ± 0.2/min), large amplitude contractions which began in the proximal colon and propagated in an anal direction (Figures 1A–C)
Summary
Our understanding of colon motility, dysmotility, and potential treatments is still in its infancy. The interstitial cells of Cajal (ICC) pacemaker system and all parts of the enteric nervous system (ENS), are critical for normal motor patterns to occur, but their structures and functions are intertwined which has made their specific roles in normal motility control and pathophysiology of dysmotility often difficult to decipher. Injury to ICC in patients with dysmotility is always associated with injury to enteric nerves (Streutker et al, 2007; Huizinga and Lammers, 2009). This makes it difficult to delineate the specific contributions of both systems to physiology and pathophysiology and it emphasizes the close connections between the two. Abnormality of ICC in many intestinal disorders is firmly established (He et al, 2000; Wang et al, 2007; Huizinga et al, 2009), the contribution of ICC to abnormal colonic motilities is still difficult to assess because of our lack of knowledge on their contribution to normal control mechanisms, in vivo
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