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Peristalsis mechanism





The esophagus is a hollow muscular tube, closed proximally and distally by muscular sphincters.The esophageal wall is composed of distinct layers. The inner mucosal layer consists of squamous epithelium and underlying connective tissue, within which lies a longitudinally oriented muscle layer called the muscularis mucosa. The function of this muscle layer is unclear, but it likely is involved in mucosal movement. The outer muscular coat, known as the muscularis propria, is involved in bolus transport and consists of an inner layer of circularly oriented muscle fibers and an outer layer of longitudinally oriented fibers. In between these two muscle layers lies the myenteric plexus, which controls the motor function of these muscles. The upper esophageal sphincter (UES) and proximal one third of esophageal body is composed of striated muscle. There is then a transition zone where striated and smooth muscle intermix. The lower esophageal sphincter (LES)  and the distal one half to two thirds of the esophageal body are composed of smooth muscle.
The main function of the esophagus is to propel swallowed food or fluid into the stomach. This occurs through sequential or "peristaltic" contraction of circular muscle in the esophageal body, in concert with appropriately timed relaxation of the upper and lower esophageal sphincters. The esophagus also must clear any refluxed gastric contents back into the stomach and takes part in vomiting and belching.

The Neuromechanichal Loop Hypothesis

As neural peristalsis is a behavior involving enteric neural circuits that are dependent on ongoing mechanical stimulation of the advancing contents, it could be considered as a self-sustaining propulsive behavior. In this study we call this description of events the “neuromechanical loop hypothesis” of neural peristalsis. This hypothesis places the enteric reflex pathways as the basis of peristalsis, and places them in a dynamic process, thus avoiding the historical misconception of peristalsis as a simple “reflex.” This hypothesis requires activation of excitatory neurons by mechanical distension to initiate the peristaltic contractions. Furthermore, once the peristaltic contractions starts, the mechanical distension, created by propulsion of content, immediately anal to the contracted region, should act as a new mechanical stimulus, activating the polarized enteric reflex pathways in sequence but displaced aborally, resulting in the peristaltic behavior with associated propulsion of contents.
Ideally, this hypothesis could be tested by recording from excitatory and inhibitory enteric motor neurons during periods of propagating contractions associated with movement of content. However, the very movements of the gut wall pose serious methodological constraints. One study that did succeeded in recording, from a fixed point, electrical activity from of smooth muscle during peristalsis in a tubular preparation had to remove the serosa and longitudinal muscle and because recording was limited to one location the site of origin of the motor neuron input could not be determined (yokoma and north ).
We have recently developed a method, combining spatiotemporal maps of gut diameter and intraluminal pressure that identifies, in tubular preparations, where the smooth muscle is being actively excited or inhibited (costa el. 2013bd) and where it is likely to be responding passively to movement of content from elsewhere. Using that technique, in this paper we provide evidence for the neuromechanical hypothesis of neural peristalsis.

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