The movements of the intestine are called peristalsis. Different movement patterns of peristalsis are distinguished. The so-called pacemaker cells of the intestine control, for example, slow potential waves in a matter of seconds or minutes.
During digestion, non-propulsive peristalsis occurs in the form of annular contractions. The transport of the intestinal contents towards the rectum takes place via propulsive peristalsis. Continuous contractions of various areas of the intestine prevent the upward migration of the intestinal contents.
The peristaltic reflex is the triggering of the characteristic intestinal peristalsis by a stretching stimulus. Physiologically, the intestinal content gives the stretch stimulus to trigger the digestive movements. The fuller the intestine becomes, the more the intestinal contents stimulate the so-called mechanoreceptors of the intestinal mucosa.
When threshold potential is exceeded, the enterochromaffin cells in the intestinal walls release serotonin. It is a messenger substance of the enteric nervous system. The serotonin excites the nerve cells of the intestinal wall and triggers muscle contractions or relaxations. Due to the messenger substance, the reflex is independent of the central nervous system and can also be observed on the isolated intestine.
In the human organism there are different, relatively independently acting nervous systems. In addition to the central nervous system, the vegetative nervous system can be mentioned. The enteric nervous system together with the sympathetic and parasympathetic nervous system form the autonomic system. The enteric nervous system is the autonomic nervous system of the gastrointestinal tract, which is close in structure to the brain. For this reason, the gastrointestinal tract is also referred to as a small brain.
Extrinsically sympathetic and parasympathetic nerve tracts monitor and regulate the intestinal motility, but ultimately the gastrointestinal tract is the only organ isolated from the central nervous system to work in the situation. All motor functions of the anatomical structure are thereby controlled quasi autonomously.
The enteric motor is a reflex motor. The digestion is therefore involuntary and independent of one's own decisions. The maintenance of all digestive movements is the task of the enteric nervous system.
For communication purposes, enteric neurons synthesize more than 25 transmitter substances. More than 1, 000 different transmitter combinations are thus theoretically available for controlling the gastrointestinal motor system. Around 30 populations function as sensory neurons, motor neurons and interneurons, and harbor neurotransmitters.
The main function of the enteric nervous system is synaptically mediated activation and inhibition. Fast-moving postsynaptic potentials are the most important transmission mechanism. Acetylcholine is the primary neurotransmitter in the enteric nervous system. It activates postsynaptic neurons by binding to nicotinic receptors. Serotonin and adenosine triphosphate also participate in mediation. Serotonin binds to 5-HT3 receptors.
The enteric nervous system regulates its effector systems through reflex circuits. The peristaltic reflex forms the propulsive peristalsis. The IPAN (intrinsic primary afferent neurons) in the enteric nervous system are stimulated by the mechanical pressure of the intestinal contents or by chemical stimuli and initiate a reflex circuit that causes a higher contraction and a lower relaxation of the circular musculature.
The projection polarity of the enteric motor neurons ensures the functioning. Inhibiting and excitatory motor neurons can be controlled directly by the IPAN. However, the IPAN can also use an intermediary interneuron for indirect activation. The interconnection runs over distances of millimeters to centimeters. Several of these circuits are activated one after the other.
Its modulation preserves the transport of intestinal contents by activating or inhibiting synaptic contacts between the circuit elements.
Pathological hyperactivities of inhibitory nerve cells in the intestine so relax the intestinal muscles that almost atony exists. The peristaltic reflex comes to a standstill in extreme cases. Even a complete paralysis of the intestine can occur in this way. The peristaltic reflex can then no longer be triggered. The resident mechanoreceptors no longer register any stimuli even with strong intestinal wall tension. The opposite state may also be of pathological significance, for example in the case of a pathological hyperactivity of the excitation system. Such hyperactivity results in accelerated transport and diarrhea.
Many diseases of the intestine are associated with functional obstruction. Some of these diseases arise on the basis of neuronal degeneration, which can take on different proportions. Generalized degeneration involves, for example, the inhibitory and excitatory nerve cell populations of the enteric nervous system. If the inhibitory nerves fail, it has more serious consequences than a failure of the excitatory cells. The inhibitory nerve cells of the intestine maintain a braking effect during intestinal movement.
By completely eliminating the inhibitory tone, conditions such as Hirschsprung's disease, achalasia, or sphincter stenosis may develop. Each of these diseases can be rooted in a local aganglionosis. Hypoganglionosis causes intestinal pseudo-obstruction. These relationships, for example, play a role as causes of Chagas disease dysfunction and cytomegalovirus infection.
Diabetes mellitus can also interfere with enteric circuits. The dysfunctions manifest themselves in this case above all in a slowed gastric emptying, which can increase up to an apparent paresis.
Neurological diseases such as multiple sclerosis do not attack the enteric, but the central nervous system. All associated intestinal disorders have sympathetic or parasympathetic cause and are not in the intestine itself.