دى ال case 4 A 32-year-old woman presents to her primary care physician’s office with difficulty chewing food. She states that when she eats certain foods that require a significant amount of chewing (meat), her jaw muscles become weak and “tired.” After a period of rest, her jaw muscles regain their strength until she eats again. The patient is diagnosed with myasthenia gravis and is started on neostigmine, an acetylcholinesterase (AChE) inhibitor. 1. What effect would an AChE inhibitor have at the neuromuscular junction? 2. How would a large reduction in extracellular [Ca2] affect synaptic transmission at the neuromuscular junction? 3. What is the ionic mechanism that underlies the endplate potential (EPP) produced by acetylcholine (ACh) release? ANSWERS TO CASE 4: 1. Effect of AChE inhibitor: Blocks the degradation of ACh, causing an increase in the endplate potential, and prolongs the action of ACh at the motor endplate. 2. Effect of reducing [Ca2]o: Reduces Ca2-dependent exocytosis of Ach from vesicles in the presynaptic terminal. 3. Ionic mechanism of EPP: ACh opens ligand-gated channels that are equally permeable to Naand K. The net effect is depolarization that reaches action potential threshold in the muscle cell.
Posted on: Sat, 27 Dec 2014 18:55:13 +0000
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