Muscle Contraction And Cell Motility

Muscle Contraction and Cell Motility

This volume intends to provide a comprehensive overview on the mecha nisms of muscle contraction and non-muscle cell motility at the molecu lar and cellular level, not only for investigators in these fields but also for general readers interested in these topics. A most attractive feature of various living organisms in the animal and plant kingdoms is their ability to move. In spite of a great diversity in the structure and function of various motile systems, it has frequently been assumed since the nineteenth century that all kinds of "motility" are essentially the same. Based on this assumption, some investigators in the nineteenth century thought that the mechanisms of motility could better be studied on primitive non-muscle motile systems such as amoeboid movement, rath er than on highly specialized muscle cells. Contrary to their expectation, however, the basic mechanisms of motility have been revealed solely by investigations on vertebrate skeletal muscles, since a monumental discovery of Szent-Gyorgyi and his coworkers in the early 1940s that muscle contraction results from the interaction between two different contractile proteins, actin and myosin, coupled with ATP hydrolysis.

Molecular Biology of the Cell

Colonic Motility

Three distinct types of contractions perform colonic motility functions. Rhythmic phasic contractions (RPCs) cause slow net distal propulsion with extensive mixing/turning over. Infrequently occurring giant migrating contractions (GMCs) produce mass movements. Tonic contractions aid RPCs in their motor function. The spatiotemporal patterns of these contractions differ markedly. The amplitude and distance of propagation of a GMC are several-fold larger than those of an RPC. The enteric neurons and smooth muscle cells are the core regulators of all three types of contractions. The regulation of contractions by these mechanisms is modifiable by extrinsic factors: CNS, autonomic neurons, hormones, inflammatory mediators, and stress mediators. Only the GMCs produce descending inhibition, which accommodates the large bolus being propelled without increasing muscle tone. The strong compression of the colon wall generates afferent signals that are below nociceptive threshold in healthy subjects. However, these signals become nociceptive; if the amplitudes of GMCs increase, afferent nerves become hypersensitive, or descending inhibition is impaired. The GMCs also provide the force for rapid propulsion of feces and descending inhibition to relax the internal anal sphincter during defecation. The dysregulation of GMCs is a major factor in colonic motility disorders: irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and diverticular disease (DD). Frequent mass movements by GMCs cause diarrhea in diarrhea predominant IBS, IBD, and DD, while a decrease in the frequency of GMCs causes constipation. The GMCs generate the afferent signals for intermittent short-lived episodes of abdominal cramping in these disorders. Epigenetic dysregulation due to adverse events in early life is one of the major factors in generating the symptoms of IBS in adulthood. Table of Contents: Introduction / Regulatory Mechanisms / Colonic Motility in Health / Colonic Motility Dysfunction / References