The gastrocolic reflex is a physiological reflex that controls the motility of the lower gastrointestinal tract following a meal. As a result of the gastrocolic reflex, the colon has increased motility in response to the stretch of the stomach with the ingestion of food. The gastrocolic reflex allows room for the consumption of more food via control over peristalsis and movement of ingested food distally toward the rectum. Myoelectric recordings demonstrate the reflex in the large intestine that shows a spike in electrical activity within minutes of food consumption. The gastrocolic reflex initiates and controls migrating motor complexes throughout the colon. These motor complexes act cyclically during the digestion process and can be broken up into four phases.

The control of these phases is multifactorial, involving neurological, mechanical, and paracrine mediators.[1] Several neuropeptides are suspected mediators of the reflex, including cholecystokinin, serotonin, neurotensin, and gastrin. Three centers of control have been identified and studied and include myogenic control, hormonal control, and neural control. The sigmoid colon is the region most affected during the phasic response of digestion, which consists of cyclical periods of contraction followed by relaxation to propel food distally toward the rectum. These contractions are generated in the myenteric plexus and accomplished by the muscularis externa — the gastrocolic reflex results in the urge to defecate after a meal. When food enters the rectum and drives pressures up, the gastrocolic reflex stimulates expulsion of the contents of the rectum via defecation.[2]

Alteration in the gastrocolic reflex has been a suspected etiology in patients with irritable bowel syndrome (IBS). Patients with IBS have demonstrated a stronger colonic response to the gastrocolic reflex. These patients may experience a strong urge to defecate following ingestion of a meal and may experience symptoms like abdominal distension, flatulence, pain, and tenesmus.[3][4] Furthermore, alternations in the gut microbiome can cause a downstream effect that alters the enteroendocrine cells' ability to sense and carry out paracrine functions, thus indirectly affecting the motility of the colon.

Profound gastrocolic reflex has been implicated in the idiopathic variant of dumping syndrome (DS). Although abdominal pain is present in both DS and IBS, systemic signs including palpitations, hypotension, dizziness, diaphoresis often accompany DS. Another key difference in the presentation of DS is that they often present with protein-calorie malnutrition due to increased excess nutritional loss in diarrhea.[5]

Both IBS and DS are caused by profound gastrocolic reflex, whereas poor gastrocolic reflex results in constipation. Neuronal dysfunction may lead to impaired gastrocolic reflex and poor gut motility. Diabetic patients with neuropathy often have gastroparesis resulting in delayed gastric emptying and also impaired gastrocolic reflex leading to constipation.[6]

The cellular makeup of the gastrocolic reflex is multisystemic and includes cell bodies from the nervous, endocrine, and gastrointestinal systems. The primary mediators are neurons of the autonomic nervous system, neurons of the myenteric (Auerbach’s) plexus, interstitial cells of Cajal, and enteroendocrine cells that line the GI tract.

Sympathetic nerve fibers contribute an inhibitory effect on the colon, while parasympathetic nerve fibers contribute a stimulatory effect. The nerve supply to the colon is broken up between midgut and hindgut derived structures. Structures derived from the midgut include the ascending colon and proximal two-thirds of the transverse colon. These midgut derived structures receive their sympathetic supply from nerves that originate from the superior mesenteric plexus and their parasympathetic supply via the vagus nerve. Structures derived from the hindgut include the distal one-third of the transverse colon, the descending colon, and the sigmoid colon. These structures receive their sympathetic innervation from the inferior mesenteric plexus and parasympathetic innervation via pelvic splanchnic nerves.

Located in between the inner and outer layers of the muscularis externa, the myenteric plexus generates and helps coordinate gut motility. A sensory component of the myenteric plexus has been identified, and this is thought to help with coordination and the propagation of migrating motor complexes. The myenteric plexus propels a food bolus distally by contracting the radius of the lumen of the bowel and extending the length of the bowel.[2] The cell bodies of nerves located in the myenteric plexus communicate using gap junctions with both an excitatory component, as well as an inhibitory component.[7]

Interstitial cells of Cajal are located between smooth muscle cells and nerve endings throughout the GI tract and are responsible for the inherent pacemaker activity of the GI system. These cell bodies interact with smooth muscle cells to transduce contributions from the enteric motor neurons and turn these signals into the stimulus needed for phasic smooth muscle cells to propel the food bolus distally.[8]

Enteroendocrine cells (EECs) are cells derived from endoderm epithelial cells that are abundant throughout the GI tract. These cells form the largest endocrine organ in the body and are responsible for many tasks, including GI secretion and motility. These cells function via endocrine and paracrine roles. They sense the contents of the lumen of the bowel and excrete neuropeptides that can act on distal organs or even act on cells nearby, including neurons of the enteric nervous system that control motility. Research has shown that EECs can act directly on cells of the enteric nervous system to help initiate and propagate the proper physiological response.[9]

The vagus nerve derives from two separate origins depending on functionality. The motor aspect of the nerve derives from the basal plate of the medulla oblongata, and the sensory aspect arises from the neural crest.[10] The neurons of the enteric nervous system derive from neural crest cells that migrate to occupy the GI tract.[11] Interstitial cells of Cajal appear to arise from mesenchymal precursor cells.[12] Enteroendocrine cells that are responsible for the management of GI hormones arise from pluripotent intestinal stem cells. These stem cells are present within intestinal crypts.[13] Smooth muscles of the colon derive from mesoderm.

The gastrocolic reflex is multisystemic in origin. The reflex involves the autonomic nervous system, the enteric nervous system, and cells of the GI tract that regulate endocrine functions. Signals from the central nervous system communicate with the enteric nervous system and vice versa controlling peristalsis. The enteric nervous system proves to be paramount and is demonstrated by the morbid effects of enteric nervous system neuropathies; this is in contrast with the importance of vagal and sympathetic inputs, which have shown not to carry as much of an effect if these connections become interrupted.[14]