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THE DIGESTIVE SYSTEM: Introduction and Upper GI

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THE DIGESTIVE SYSTEM: Introduction and Upper GI THE DIGESTIVE SYSTEM: Introduction and upper GI Dalay Olson Ph.D Office: Jackson Hall 3-120 Salivary glands Oral cavity Pharynx Lecture 1 Esophagus Upper GI Stomach Liver Lecture 2 Gastric Physiology Pancreas Small intestine Large intestine Today’s Lab, Lecture 3 & 4 SI, liver, pancreas and LI LEARNING OBJECTIVES 1. Identify the layers of the gut wall and describe the function of each layer 2. Explain the modulation of the enteric nervous system by the neurotransmitters of the autonomic nervous system 3. Explain how the enteric nervous system serves as a control center for short reflexes 4. Explain the relationship between the basal electrical rhythm (BER) in gut smooth muscle, the production of action potentials by additional stimuli and the production of tension in the gut muscularis. 5. Predict the effects stretch, NE, Epinephrine, Atropine, Physostigmine, K+ and BaCl2 will have on the small intestine tissue. Understand the underlying mechanism of the stimuli above and how they induce changes in small intestine motility. (This learning objective is NOT listed in the course packet, but you need to know it for the exam!!) Muscularis Externa: Longitudinal muscle Circular muscle IMPORTANT GUT LAYERS Mucosa: Epithelium Lamina propria Muscularis mucosae Serosa: Submucosal plexus Epithelium Myenteric plexus Connective Tissue Submucosa: Enteric Nervous System: ORGANIZATION OF THE ENTERIC NERVOUS SYSTEM Enteric Nervous System To CNS Myenteric Plexus Long Reflex Interneuron Submucosal plexus Short Reflex Sensory Neuron Longitudinal and Exocrine cells Mucosal circular smooth and endocrine epithelium muscle layers cells Extrinsic neuronal input NERVOUS SYSTEM BRANCHES AND THEIR EFFECTS ON MOTILITY Enteric Nervous System (ENS) – Contains the interneurons that can serve as a control center for short reflexes – Responds to extrinsic (CNS) neuronal input from SNS and PNS. Sympathetic nervous system (SNS) – Postganglionic neurons release norepinephrine – Tends to inhibit digestive activity Parasympathetic nervous system (PNS or Vagus nerve) – Postganglionic neurons release acetylcholine – Tends to stimulate digestive activity – The Vagus nerve is the most important parasympathetic contributor. MOTILITY PERISTALSIS SEGMENTATION Peristalsis 2 MAJOR JOBS OF INTESTINAL MUSCLE Thoroughly mixing food molecules Moving contents along intestine Segmentation TYPES OF MOTILITY IN THE SI Extrinsic (CNS) neuronal input • Sympathetic innervation inhibits motility in the gut. • Parasympathetic innervation activates motility in the gut. • Modulates the resting membrane potential of a pacemaker cell to inhibit or activate motility Myogenic Reflex • Individual smooth muscle contracts in response to stretch. • Increased stretch opens mechanically gated Ca2+ channels → increased force of contractions • Independent of ENS Intrinsic (ENS) neuronal input (two examples below) • Mechanoreptors on sensory nerves sense stretch and activate interneurons. Interneurons activate the myenteric plexus causing muscle contraction. • Chemoreceptors on sensory nerves sense acid in the intestine and activate interneurons. Interneurons then activate the submucosal plexus causing excrete bicarbonate to neutralize the acid. Spontaneous • Contractions of the smooth muscle occur as a result of the oscillating membrane potential (BER). • Contractions occur even when food is not present in the intestine. • The migrating motor complex (MMC) is activated in fasting individuals. • Contractions help sweep any undigested food through the digestive system. Spontaneous PACEMAKER CELLS! SMOOTH MUSCLE CONTRACTION SMOOTH MUSCLE CELLS! WHAT WE WOULD HAVE DONE…EXPERIMENTAL CONDITIONS • The 95% O2 and 5% CO2 • Krebs/Ringer Bicarbonate solution (Physiological interstitial fluid) • Experiment is running at 37˚Celsius (body temperature) • What are we measuring? • Displacement. How much is the tissue moving. The machine isn’t calibrated so we can’t calculate force. We are only measuring a relative change in position. An increase in the displacement is an increase in contraction. STIMULI YOU SHOULD UNDERSTAND FOR THE EXAM • Stretch of the tissue • Acetylcholine (Ach) • Epinephrine • Physostigmine—AchE inhibitor • Atropine—Blocks Ach Receptor • K+ • BaCl2—Blocks K+ channel Myogenic Reflex STRETCH Stretch Ca2+ Ca2+ Channel Opens up Ca2+ channels that increase strength of contraction Stretch activates and opens mechanically gated Ca2+ channels. Ca2+ comes into the smooth muscle cell and the cell contracts. ACH, PHYSOSTIGMINE & ATROPINE Parasympathetic What does Acetylcholinesterase do? Ach binding Atropine activates blocks Ach intracellular Receptor, Ca2+ release. inhibiting Ach Increasing binding. motility! Decreases motility! AchE inhibitors (Physostigmine) What wouldAcetylcholine happen activatesif you didn’t motility have AchE? keep Ach levels high in near the smooth muscle cells. Increases motility! NE/EPI Sympathetic NE or Epi binding inhibits intracellular Ca2+ release. Decreasing motility! Epinephrine inhibits motility ELEVATED EXTRACELLULAR K + How does extracellular fluid composition affect depolarization? K+ K+ K+ DepolarizingK+ the membrane will open K+ K+ voltage gatedK+ Ca2+ channels, allowing K+ K+ Ca2+ into theK+ cell. Increased motility!K+ K+ K+ K+ K+ Increasing extracellular [K+] depolarizes the cell by preventing K+ from exiting. BARIUM CHLORIDE (K+ CHANNEL BLOCKER) What effect would blocking the K+ channel have on membrane potential? Blocking K+ channels will depolarize the membrane, opening voltage gated Ca2+ channels and allowing Ca2+ into the cell. How would this change gut motility?.
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