GI Motility Flashcards
4 basic GI processes
Motility
Secretion
Digestion
Absorption
2 broad categories of motility
Mixing movements
Propulsive movements
Mixing movements
Redistribute luminal contents locally
Enhancing the exposure to digestive secretions
Expose luminal contents to GI tract absorbing surfaces (epithelium)
Propulsive movements
Move the luminal contents forward
Rate of propulsion varies with specific function of region (esophagus = fast, SI = slow)
Myenteric plexus
Also called Auerbach’s plexus
Lies between circular and longitudinal muscle layers
Coordinated muscularis-externa contractions
What type of muscle is in the GI tract?
Smooth muscle
Have gap junctions between them for electrical continuity
How do the muscle cells contract?
Contraction is initiated by increased cytoplasmic Ca
Sarcoplasmic reticulum associated with PM at indentations (calvaeoli)
Contractile acto-myosin filaments are obliquely arranged
Cytoskeletal filaments are anchored at dense body junctions
Cells are physically and electrically coupled at gap junctions
Thick Filament regulation
When intracellular Ca concentration is increased, Ca binds to calmodulin
Ca-calmodulin complex activates Myosin Light Cain Kinase
MLCK phosphorylates myosin so it can bind to actin (begins the shortening process)
The phosphate is removed by Myosin Light Chain Phosphatase
De-phosphorylated myosin can no longer bind to the actin filament and the contraction is terminated
What are the 2 ways that Ca is released?
Depolarization of the membrane
Production of IP3 at the PM (stimulated by hormones and NTs)
How does depolarization lead to muscle contraction?
Cell is depolarized via synaptic transmission
Voltage gated Ca channel is in the base of the caveolae, allows some Ca to enter
Ca binds ryanodine receptor on SER
Huge efflux of Ca into the cytoplasm
How does the production of IP3 lead to muscle contraction?
Hormones and NTs bind at the sarcolemma
IP3 is produced, and diffuses into the cell
Binds to the IP3 receptor on the SER
Ca diffuses out of the SER into the cytosol
How is the Ca removed from the cytoplasm?
Ca ATPases
On the sarcoplasmic membrane
On the SER
4 factors that regulate the GI system
Intrinsic electrical properties of smooth muscle cells
Enteric NS
Autonomic NS
Other systems (brain, immune, hormones)
Interstitial cells of Cajal
Non-contractile pacemaker cells
Specialized smooth muscle cells that undergo spontaneous, transient membrane depolarizations
The depolarizing potentials are termed slow waves
Propagate through gap junctions (smooth muscle network)
How are the duration and amplitude of slow waves modulated?
By neurotransmitters/agonists that are released by enteric motor neurons in the wall of the GI tract
How do slow waves cause APs?
If slow wave depolarizations reach AP threshold, a burst of APs result
The number of APs is proportional to the duration the slow wave remains above the threshold
Greater number of APs = greater elevation of intracellular Ca = greater strength of contraction of muscle cell
2 ways the ENS functions
Via electrical communication and the release of NTs
Can operate without external input (brain), so is considered reflexive
Made up of the submucosal and myenteric plexus
3 components of the ENS
Sensory neurons (including mechanoreceptors, chemoreceptors, and osmoreceptors) Interneurons (excitatory and inhibitory) Secretomotor cells (influence smooth muscle, epithelial cells that secrete/absorb fluid, enteric endocrine cells)
3 functions of the ANS in the gut
Influences ongoing ENS activity
Directly affects smooth muscle and glands
Alters GI hormone levels
Pre and post ganglionic fiber locations with the
- Sympathetic NS
- Parasympathetic NS
- Preganglionic fibers synapse in ganglia, post ganglionic (NE) synapse in the ENS
- Preganglionic fibers synapse with a postganglionic fiber (ACh) within the ENS
Smooth muscle En Passant innervation
Motor axons have multiple varicosities (swellings containing packets of NT)
Release the transmitter in the vicinity of smooth muscle
NT diffuses to its targets
Parasympathetic vs sympathetic function in GI
Parasymp: increases motility and secretions, relaxes sphincters (occurs during and immediately after a meal)
Symp: decreased motility and volume of secretions, contracts sphincters (during stress response)
Where is the ‘swallowing center’?
Medulla oblongata
3 phases of swallowing
Oral
Pharyngeal
Esophageal
Oral phase of swallowing
Pushing a food bolus towards the back of the oral cavity and up against the palate
Requires the tongue
Initiation of swallowing is voluntary, but once initiated it becomes reflexive (next stage)
Pharyngeal phase of swallowing
Pharynx is located at the posterior of the oral cavity, at its junction with the nasal passages
Touch and pressure receptors in the pharyngeal palate are activated by the food bolus
Info is sent to the medulla via the trigeminal nerve
This initiates the reflexive component of swallowing
Once the trigeminal nerve is activated, the swallowing reflex begins. What does this entail?
Contraction of the pharyngeal wall behind the bolus pushes food toward the esophagus
Tongue position prevents the bolus from travelling back into the mouth
Uvula elevates to seal the nasal passages
Vocal cords contract and the epiglottis closes over the trachea
Swallowing center inhibits respiratory center in brain
Pharyngoesophageal sphincter
Top of the esophagus
Remains closed except during swallowing to prevent air entering the stomach
Esophageal phase of swallowing
Swallowing center relaxes the pharyngoesophageal sphincter
Swallowing center then initiates primary peristaltic waves by interacting with the EN
Primary peristalsis
Inner circular layer contracts, pinching a ring
Outer longitudinal layer contracts in front, reducing the tube length
Primary peristaltic wave takes 5-9 seconds to travel from the beginning to the end of the esophagus
Secondary peristalsis
Reflexive
Does not involve the swallowing center
Luminal contents become lodged, the distension of the Gi wall activates stretch receptors, they stimulate the ENS, the ENS coordinates a strong peristaltic wave to dislodge the luminal contents
Sweeper of the esophagus
Gastroesophageal sphincter
Opens when a peristaltic wave pushes a food bolus against this region
Reflexive relaxation
Mediated by the vagus nerve
Contracts after to prevent reflux
2 parts of motility in the small intestine
Segmentation (mixing during meals)
Migrating mobility complex (moves contents in between meals)
ENS controls both
Segmentation
Alternating contractions and relaxations of adjacent sections of the small intestine
Initiated by distension of lumen, presence of gastrin, parasympathetic input
Helps move chyme toward LI
Migrating motility complex
Begins at the duodenal/gastric junction
Consists of weak peristaltic contractions that travel for a short distance
Second wave begins slightly more distally than the initiation site of the first wave, and travels slightly further
Takes about 2 hours to get from stomach to LI
