Physiology chapters
Enteric nervous system, slow waves and GI hormones
How the gut wall is organised, the myenteric and submucosal plexuses, the electrical slow waves and spike potentials of gut smooth muscle, and the main gastrointestinal hormones with their sources, stimuli and actions.
- The gut wall has its own nervous system: the myenteric (Auerbach) plexus controls movement; the submucosal (Meissner) plexus controls secretion and blood flow; parasympathetic nerves stimulate, sympathetic nerves inhibit.
- Gut smooth muscle has slow waves set by the interstitial cells of Cajal; contraction happens only when spike potentials (Ca2+ entry) ride on top of them.
- Key hormones: gastrin (acid), CCK (gallbladder and enzymes), secretin (bicarbonate), GIP (insulin), motilin (migrating motor complex).
On this page
Overview
The gastrointestinal tract moves food along, mixes it, secretes digestive juices and absorbs nutrients. To do this it has:
- A layered wall with smooth muscle.
- Its own enteric nervous system, influenced by autonomic nerves.
- Hormones released from cells in its lining.
Layers of the gut wall
From the inside out:
- Mucosa: epithelium, lamina propria, muscularis mucosae.
- Submucosa: connective tissue with the submucosal plexus.
- Muscularis externa: inner circular and outer longitudinal muscle, with the myenteric plexus between them.
- Serosa (or adventitia).
The enteric nervous system
The "brain of the gut": about as many neurons as the spinal cord. It can work on its own, even when cut off from the CNS.
| Plexus | Position | Main role |
|---|---|---|
| Myenteric (Auerbach's) | Between longitudinal and circular muscle | Motility: tone, strength and rate of contractions, peristalsis |
| Submucosal (Meissner's) | Submucosa | Secretion, absorption and local blood flow |
Transmitters include acetylcholine (mostly excitatory), and inhibitory transmitters such as VIP and nitric oxide, which relax sphincters and allow receptive relaxation.
Myenteric plexus = motility. Submucosal plexus = secretion.
Autonomic control
- Parasympathetic (mainly the vagus to the transverse colon; pelvic nerves S2–S4 for the rest): increases motility and secretion.
- Sympathetic (T5–L2, through prevertebral ganglia): inhibits motility and secretion, constricts sphincters and reduces blood flow.
Reflexes
- Local reflexes within the enteric system (secretion, peristalsis).
- Gut-ganglia-gut reflexes through sympathetic ganglia: for example the gastrocolic reflex (food in the stomach stimulates colonic movement) and the enterogastric reflex (distension or acid in the duodenum slows the stomach).
- Gut-brain-gut reflexes through the vagus and spinal cord: for example vomiting and defecation.
Gastrointestinal smooth muscle
- Small, spindle-shaped cells joined by gap junctions, so they act as a functional syncytium (single-unit smooth muscle).
- Contraction is triggered by Ca2+ entry, which binds calmodulin and activates myosin light-chain kinase.
- They can maintain long, steady contractions (tonic) or rhythmic contractions (phasic).
Slow waves and spike potentials
Slow waves
- Slow, rhythmic changes in membrane potential (about 5–15 mV) that occur all the time.
- Generated by interstitial cells of Cajal, the pacemaker cells of the gut.
- They are not action potentials and usually do not by themselves cause contraction (except partly in the stomach).
- Their frequency sets the maximum rate of contraction in each region.
| Region | Slow-wave frequency (approx.) |
|---|---|
| Stomach | 3 per minute |
| Duodenum | 12 per minute |
| Terminal ileum | 8–9 per minute |
Spike potentials
- True action potentials that occur at the peaks of slow waves when the membrane is depolarised beyond about −40 mV.
- Caused mainly by calcium-sodium channels that open slowly and stay open longer than nerve channels.
- Each burst of spikes produces a contraction; the more spikes, the stronger the contraction.
Slow waves set the rhythm; spike potentials cause contraction.
What changes excitability
- More excitable (depolarised): stretch, acetylcholine, parasympathetic stimulation, some gut hormones.
- Less excitable (hyperpolarised): noradrenaline and adrenaline, sympathetic stimulation.
Gastrointestinal hormones
| Hormone | Source | Main stimulus | Main actions |
|---|---|---|---|
| Gastrin | G cells of the gastric antrum (and duodenum) | Protein (peptides, amino acids) in the stomach; stomach distension; vagal stimulation (GRP) | ↑ Gastric acid; growth of gastric mucosa; ↑ gastric motility |
| Cholecystokinin (CCK) | I cells of the duodenum and jejunum | Fats and amino acids in the duodenum | Gallbladder contraction; ↑ pancreatic enzyme secretion; relaxes the sphincter of Oddi; slows gastric emptying; satiety |
| Secretin | S cells of the duodenum | Acid in the duodenum | ↑ Pancreatic and biliary bicarbonate; ↓ gastric acid |
| GIP (glucose-dependent insulinotropic peptide) | K cells of duodenum and jejunum | Glucose, fat, amino acids | ↑ Insulin release; ↓ gastric acid |
| Motilin | M cells of duodenum and jejunum | Fasting (released in cycles) | Starts the migrating motor complex |
| Somatostatin | D cells of stomach, duodenum and pancreas | Acid; many | Inhibits almost all gut hormones and secretions |
| Ghrelin | Stomach | Fasting | Hunger; GH release |
| GLP-1 | L cells of ileum and colon | Nutrients | ↑ Insulin; slows gastric emptying; satiety |
Secretin responds to acid and releases bicarbonate; CCK responds to fat and contracts the gallbladder.
Gastrin is made mainly in the antrum, not the body, of the stomach. The acid-secreting parietal cells are in the body and fundus.
Clinical relevance
Zollinger-Ellison syndrome
How it happens: a gastrin-secreting tumour (gastrinoma), usually in the pancreas or duodenum.
What you see: very high acid, multiple or unusual peptic ulcers, diarrhoea.
Hirschsprung disease
How it happens: absence of enteric ganglion cells (neural crest failed to migrate) in the distal colon.
What you see: a contracted, aganglionic segment that cannot relax, with a dilated colon above it; delayed passage of meconium.
Achalasia
How it happens: loss of inhibitory neurons (nitric oxide, VIP) in the myenteric plexus of the lower oesophagus.
What you see: the lower oesophageal sphincter fails to relax; difficulty swallowing both solids and liquids.
Expect: the role of each plexus, parasympathetic vs sympathetic effects, interstitial cells of Cajal, the difference between slow waves and spike potentials, slow-wave frequencies, and the source, stimulus and action of gastrin, CCK, secretin, GIP and motilin.
Quick revision
- Myenteric plexus: motility. Submucosal plexus: secretion and blood flow.
- Parasympathetic stimulates; sympathetic inhibits.
- Interstitial cells of Cajal make slow waves; spikes cause contraction.
- Slow waves: stomach 3/min, duodenum 12/min, ileum 8–9/min.
- Gastrin (antrum G cells): acid. CCK (I cells): gallbladder, enzymes. Secretin (S cells): bicarbonate.
- GIP: insulin. Motilin: migrating motor complex. Somatostatin: inhibits.
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What is the function of the myenteric plexus?
It mainly controls gut motility: the tone, rhythm and strength of contractions.
What are slow waves?
Rhythmic changes in the membrane potential of gut smooth muscle, generated by interstitial cells of Cajal, that set the maximum frequency of contractions.
What stimulates secretin release?
Acid entering the duodenum.
What does cholecystokinin do?
It contracts the gallbladder, increases pancreatic enzyme secretion and slows gastric emptying.