Gut Innervation Flashcards
Visceral Afferents + 3 Locations of Their Cell Bodies + Where do their axons go form there?
Gather info (nutrients, stretch, chemical irritants, thermal stim) from viscera and give some input to enteric plexus and rest to CNS using SEROTONIN
1- Submucosal Plexus - in gut wall itself –> axons synapse right into myenteric plexus (to regulate motility) and w/in submucosal plexus (to regulate secretion)
2- Inferior/Nodose Ganglion of Vagus - give input to CNS –> axons synapse in Nucleus Tractus Solaritus (integration -vomiting center) OR area postrema (chemotactic trigger zone for nausea - in wall of 4th ventricle of medulla w/o BBB so senses direct blood-borne agents too)
3- DRG - spinal afferents that sense low and high intensity mechanical stimuli; convey PAIN INFO
Visceral Efferents
- Parasympathetic - (craniosacral) from dorsal motor nucleus of vagus OR pelvic neurons (S2-S4) –> pre-ganglionic goes all the way to wall of organ (ENS or sphincters) –> post-ganglionic right in organ
- Both Ach
- Blocked by atropine
- Sympathetic - (thoracolumbar) from T5-L2 –> paravertebral gang (symp chain) –> prevertebral gang (celiac, superior mesenteric, inferior mesenteric)
- Ach then NE at blood vessel walls
- Mainly alpha-1 vasoconstriction not direct innervation of gut
4 Components of the Enteric NS
1- Afferents - primarily use serotonin and substance P (mainly during inflammation and pain)
2- Excitatory Efferents - cause depolarization and EPSP to contract behind bolus - using Ach and sometimes substance P (project orally)
3- Inhibitory Efferents - cause hyperpolarization and IPSP to suppress contraction in front of food using NO and VIP (project anally)
4- Interneurons - integrate info then synapse on excitatory and inhibitory neurons of ENS - DRUG targets
Hirschprung Disease
- paralytic sigmoid colon due to incomplete migration of neural crest cells (do not go all the way to colon); no relaxation or peristalsis
- Neural crest cells make up whole ENS
How do opioids affect motility?
- bind mu type receptors at interneuron and inhibitory ENS synapse –> blocks this inhibitory signal
- causes inc contractility in that place BUT dec coordination –> constipation (“churning in place”)
- “Opioid constipation”
How does Cisapride affect motility?
- serotonin receptor agonist –> activation of synapse b/n interneuron and excitatory ENS cell –> inc motility
Slow Wave
- Electrical Pattern
- Interstitial Cells of Cajal - pacemakers of electrical slow wave w/o neural input; create constant depolarization -repolarization but only leads to action potential if reaches certain threshold
- Create intrinsic contractile rhythm (varies in ea area of gut) - may not reach AP w/ ea wave but rate of APs cannot exceed this rate
- Stomach = 3 waves/min
- SI = 11-12 waves/min
- Colon = 2-13 waves/min (variable)
Peristalsis
- coordinated contraction and relaxation in feeding and digestive state
- Rate determined by electrical slow wave
- Oral Ach/substance P; anal NO/VIP (excitatory and inhibitory cells at ea part of the gut but activated in a coordinated fashion so this wave moves progressively down the gut) w/ synaptic gates between
- Can be run on own w/o CNS input but vagal response to swallowing, distention and mucosal brushing can start these motor patterns
Physiological Ileus
- state of the gut most of the time (when not feeding/digesting)
- active inhibitory state (inhibitory neurons active) to maintain relaxed gut
- AKA tonic IPSPs thru most of the gut
How is sphincter tone maintained? How are sphincters opened?
- Tonically closed via smooth muscle latch mechanism - latch bridges (myosin stays attached despite dephosphorylation) and reduced # myosin light chain phosphatases that normally remove P in sphincters
- Opened by high vagal activity/distention of gut wall –> NO release by inhibitory neurons
Migrating Motor Complex (3 phases, what initiates it? function)
- Main pattern of unfed/fasting state (once digestion and absorption is complete)
- Gut at rest for ~80 min then ~20 min of three phase MMC then repeat
- Phase 1- physiological ileus (no contractions)
- Phase 2 - advancing front of irregular contractions
- Phase 3 - advancing front of regular contractions
- Initiated by local input - motilin (erythromycin - abx) or ghrelin in antrum AND from serotonin or somatostatin in duodenum
- Function = clean gut by propelling bile acid, sweeping debris, clear bacteria
- Absence can lead to gastroparesis, intestinal pseudo-obstruction or bacterial overgrowth
Segmentation
- Promotes digestion and absorption in fed state
- Propulsion in both directions but bordered by inhibitory gates so get churning/mixing in single place (for physical breakdown)
- Largely in colon
- Driven by vagal input that terminates MMC pattern
