1. short pre-ganglionic nerve fibers from the thoracolumbar region
2. through the prevertebral ganglion
   1. celiac
   2. superior mesenteric
   3. inferior mesenteric
3. post ganglionic nerve fibers targets
   1. ENS (presynaptic inhibition)
   2. musculature of sphincters
   3. blood vessels

1. preganglionic fibers from cranial and sacral region of spinal cord
2. releases ACh on postgangloionic cell body
3. postganglionic fibers project close to or within the body
4. ACh released and act on muscarinic receptor

vagus N.

pelvic N.'s

• excitatory
  • ACh
  • substance P
• inhibitory
  • VIP
  • NO

• distal large bowel
  • sigmoid
  • rectum
  • anus

• inhibit secretion, motor function of gut
• paralyze motor function and reduce splanchnic blood flow to sphincter muscle

• excitatory to secretion and motor function of gut

1. one preganglionic fiber projects to adrenal medulla without synapsing on post ganglionic fiber
2. releases ACh
3. adrenal medulla release epinepherine, norepinephrine

• smooth muscle
  • sensitive to mechanical distension of gut
• mucosa
  • sense luminal concentration of nutrients, chemicals, mechanical stimuli

• stimulates motilin secretion, leading to large propagating contractings and gastroparesis

• antagonist of dopamine 2
• inhibits interneurons, preventing reflex and gastroparesis

• ACh agonist
• stimulates M3 receptors, promoting peristalsis

• 5 HT3 antagonists (block release from enterochromaffin cells)
• reduce motility, tone, secretion, gut sensitivity

• antagonist of somatostatin
• inhibit motility, secretion, neuroendocrine peptide release
• promote phase III of digestion (intestinal phase)

• opiate agonist
• relax longitudinal muscle, contract circular muscle to reduce transit through GI and inhibit secretion

• muscarinic antagonists
• inhibit motility
• prevent ACh release from neurons (botulinum- blocks for up to 12 months)

• during development, there was no migration of neural crest cells to a particular segment in the colon
• leads to one section of the colon being tonically contracted

• no inhibitory motor neurons in the smooth muscle of the LES
• leads to a tonically contracted LES

• myenteric (btw longitudinal and ciruclar smooth muscle)- motor activity
• submucusal (btw circular smooth muscle and submucosa)- secretion, absorption, blood flow

1. ENS (performs integrative functions independently of extrinsic nerves)
2. prevertebral ganglia
3. central symp. centers
4. central parasymp. centers
5. higher brain centers that integrate functions of sympathetic and parasympathetic systems

• vagal activation- anti-inflammatory
• sympathetic activation- proinflammatory

• increase gastric acid secretion
• increased motility
• increase in mucosal coloration

1. cell body senses from ENS and sends a signal via afferents
2. goes to dorsal motor nucleus of the vagus and the NTS
3. send signal down the efferents of the vagus
4. stimulates gut response

gastrin

CCK

• They can both act on the others receptor, and they have the same second messanger: calcium.
• This leads to increased enzyme secretion from pancreatic acinar cells.
• increase cGMP can enhance increase in calcium. 

ACh uses this same method.

secretin

VIP

glucagon

GIP

Each can act on the others receptor, and they share the same second messanger: cAMP. This leads to increas enzyme release.

• GIP (K cells)- control fat metabolism
• GLP (L cells in small intestines)- increase insulin secretion and improved glucose homeostasis

• fat can be detected in the ilium.
• this causes the release of NPY, GLP-1, PYY, Neurotensin from cells in the ilium
• this will slow gastric and intestinal motility

Allows for management of postprandial glucose levels

• I could add to drugs from two different families
• their actual effect when given together is greater than the anticipated arithmetic sum of their action
• this is due to stimulation of different intracellular pathways

feeding center

satiety center

1. when sensing hypoglycemia, orexins released to NTS
2. stimulates feeding center

• when leptin levels are low (during fasting), ghrelin increases to stimulate feeding center
• when leptin levels are high, this will inhibit the feeding center

• it is tonically active
• stimulate stomach contractions
• sense food via mechanoreceptors and chemoreceptors

• CCK
• GRP
• epi

When the satiety center is stimulate, this halts the tonic activity of feeding center.