GI motility is the movement of food and associated materials through the GI tract. Motility of the GI tract occurs due to the contraction of GI muscles. Actually GI tract motility serves two purposes
- serves to move food from mouth to anus
- Serves to mechanically mix the food eventually breaking the food into smaller particles. This increases the surface area of the food exposed to digestive enzymes
The different layers (i.e. circular and longitudinal layers) of GI smooth muscles are responsible for gastrointestinal motility.
GI smooth muscles contract spontaneously: they can contract in the absence of extrinsic innervation
GI smooth muscles show intrinsic electrical rhythm along their membranes. The intrinsic rhythm occurs due to slow but continuous excitement of the muscle fibers of the GI tract. This electrical activity is both intrinsic and spontaneous. The enteric nervous system initiates and controls the intrinsic contractions of the GI smooth muscles; however, neurocrines, paracrines as well as classical hormones can modulate the force and duration of these contractions.
Gastrointestinal smooth muscles contract as a syncytium
Fibers of GI smooth muscle arrange themselves into bundles and a bundle of GI smooth muscle may contain up to 1000 individual smooth muscle fibers arranged in parallel.
Each bundle of GI smooth muscle composes of smooth muscle fibers electrically connected by gap junctions along the length of the GI tract. This arrangement enables electrical signals responsible for muscle contraction to spread readily from fiber to fiber within a particular bundle. The spread occurs both sideways and along the length, however, the spread along the length is more rapid. Moreover, smooth muscle fibers of different bundles make connections with one another at many points so that GI smooth muscles of the circular layer functions as a syncytium and GI smooth muscles of the longitudinal layer also functions as a syncytium.
Smooth muscle fibers of the longitudinal layer extend longitudinally along the length of the gut, whereas fibers of the circular muscle layer extend round the gut (wrapping round the gut).
Due to this syncytial arrangement, an action potential elicited at any point within the muscle mass spreads in all direction in the muscle. The excitability of the muscle determines how far the action potential travels; it may stop after few millimeters, at other times it may travel many centimeters or may even travel the entire length of the gastrointestinal tract.
The implication is that the circular muscle layer can contract as a single unit while the circular muscle layer can equally contract as a single unit. Nevertheless, few gap junctions connect fibers of the longitudinal muscle layer with fibers of the circular muscle layer and this enables the excitation of these layers to excite the other concomitantly.
Slow wave potentials in GI smooth muscles
Slow waves are not action potentials though they constitute cyclical depolarization and repolarization of the membrane of a smooth muscle cells. This cyclical depolarization and repolarization result from undulating changes in the resting membrane potential. GI smooth muscle cells have an unstable resting membrane potential of -50mV to -60mV. If the slow wave potential rises above -40mV, spike potentials (true action potentials) appear superimposed on the peak of the slow wave.
The frequency of slow waves determines the rhythm of most GI rhythmic contractions. Though scientists are yet to understand in details the exact cause of slow waves current knowledge holds that slow waves occur due to complex interactions among GI smooth muscle cells and specialized cells called interstitial cells of Cajal.
Slow wave is similar to cardiac muscle pacemaker potential; however both have two significant differences:
- Slow waves occur at a much slower pace compared to cardiac pacemaker potentials. Slow waves occur at a rhythm of 3 to 12 waves per minute (3/min in the stomach and 12/min in the duodenum) whereas myocardial pacemaker cells fire at a rate of 60 to 90 waves per minute.
- The second significant difference between GI slow waves and myocardial pacemaker potential is that myocardial pacemaker potential always depolarize to threshold and results in an action potential whereas not all slow wave potentials result in action potential. Sometimes, GI smooth muscle cells just cycle through series of sub-threshold slow waves, which is unable to trigger the muscle cell to fire action potentials.
Thus, not all slow waves reach threshold potentials, and a slow wave that does not reach threshold potential will be unable to cause contraction of the GI smooth muscles.
The frequency of slow waves varies by region along the gastrointestinal tract.
The stomach has the lowest frequency of slow waves: with slow waves occurring at the rate of about three (3) waves per minute whereas the duodenum has the highest frequency of slow waves, with slow waves occurring at the rate of about twelve (12) waves per minute.
Interstitial cells of Cajal act as GI smooth muscle pacemakers
Current knowledge on GI motility shows that specialized mesenchymal cells with smooth muscle-like properties called interstitial cells of Cajal (ICC) act as pacemakers for GI smooth muscle slow waves. The depolarization that arises from the ICC spread to adjacent and neighboring muscle fibers through gap junctions. Remember that GI smooth muscles arrange themselves in groups of single-unit smooth muscles with each fiber of a group electrically connected to adjacent fiber through gap junctions. Thus, GI smooth muscles form syncytiums similar to the syncytium formed by cardiac muscles.
Thus, the basic rhythm of slow wave potentials arises from the interstitial cells of Cajal rather than the GI smooth muscles themselves.
These cells get their name after a Spanish neuroanatomist Santiago Cajal. Interstitial cells of Cajal are present in the muscularis externa, muscularis mucosa, and in the two nerve plexuses of the enteric nervous system.