Feeding circuits

Describe the different roles of the myenteric and submucous plexus.

The myenteric plexus controls motor functions like peristalsis and contains sensory neurons that detect mechanical changes. The submucosal plexus senses chemical contents like nutrients and has motor neurons that regulate glandular secretions including the release of digestive enzymes

What is unusual about the parasympathetic postganglionic neurons of the enteric nervous system?

parasympathetic postganglionic neurons are located in the walls of the gut and do not have a distinct ganglia located outside the target organ

Explain why extreme bloating or distention of the GI tract can lead to pain perception in the skin of the abdomen.

this occurs because visceral and somatic sensory afferents converge onto the same secondary afferent creating referred pain

We are usually unaware of mechanical or chemical stimulation of sensory afferents in the digestive system & when we are, it is often hard to localize the sensation. Why?

we have difficulty locating visceral sensations due to fewer neurons with very large receptive fields. additionally, information is sent to the insular cortex which provides vague feedback

What are 2 broad classes of signals from the gastrointestinal tract that contribute to the desire to end a meal?

mechanical signals (distention) and chemical signals (nutrient detection and hormone release)

Why do meals with a higher caloric content make us feel more satiated longer?

they trigger a greater and more rapid release of CCK and GLP-1

Based on what we learned in class, do cholecystokinin (CCK) and Intestinal Glucagon Like Peptide 1 (GLP-1) enhance gastric emptying or delay gastric emptying?

delay gastric emptying to optimize nutrient digestion, regulate blood sugar, and promote satiety

Gastric distention and post-gastric signals contribute to the desire to end a meal. In addition to affecting our desire to eat, what else can result from activation of sensory cells detecting these signals?

activation of sensory cells can trigger gallbladder/pancreas activity, affect autonomic motor responses, and if toxins are detected trigger vomiting

Cholecystokinin is a likely satiety signal. Explain how detection of nutrients in the GI tract leads to release of this signal. Also explain where it comes from and where it goes.

nutrients bind to GPCRs on enteroendocrine cells in the intestinal epithelium which triggers an intracellular cascade to release CCK via exocytosis. CCK comes from enteroendocrine cells in mucosa of the small intestine and enters portal circulation or binds the cck receptors that lead to the nucleus of the solitary tract

Explain how Enteroendocrine L cells detect sugars. What is unusual about the receptor in these cells (where else is it found)? What do EEC type L cells released when stimulated and where does it go?

Enteroendocrine cells use specific GPCRs that are the exact same as those found in taste buds. When stimulated they release GLP-1 that enters portal circulation or binds to receptors that induce fullness

Besides cholecystokinin and GLP-1, what other substances to gastrointestinal vagal afferents detect & where do these come from?

vagal afferents also detect leptin, ghrelin (hunger), peptide YY (gastrointestinal tract), insulin, and other nutrients

Fill in the blanks: The visceral (inferior part) of the nucleus of the solitary tract (NST) receives information from what 3 neurons/classes of neurons ________________________________________________________. These neurons provide information about the mechanical state of the gut and about gut contents. The NST also directly senses circulating __________________, including glucose and amino acids in the blood. The latter is possible because the blood brain barrier is specialized in the ___________________________ (specific name) which allows sensory neurons in the NST to detect nutrients in the blood.

vagal, glossopharyngeal, and second order visceral afferents; nutrients; area postrema