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Phys Exam 1: Ch7
Excitation of Skeletal Muscle
| Question | Answer |
|---|---|
| Describe initiation of a muscle contraction | 1. AP reaches end of axon; 2. ACh is released @ NMJ; 3. ACh initiates an AP in the sarcolemma; 4. AP causes release of Ca from the SR; 5. Intracellular Ca initiates muscle contraction |
| Describe the Neuromuscular Junction (NMJ) | 1. A motor neuron axon ends at an axon terminal on a muscle fiber; 2. Each axon terminal is embedded into the surface of the muscle fiber; 3. This location is called the Motor End Plate. |
| What is the synaptic cleft? | b/n the axon terminal and the muscle fiber; ~20-30nm wide |
| What is a subneural cleft? | folds in the muscle fiber surface below the axon terminal |
| What are the components of an axon terminal? | Voltage-gated Ca channels, Vesicles of NT (ACh) |
| Describe the process of events that occur in the axon terminal in regards to Ca and ACh | 1. An AP opens Ca channels; 2. Ca influx causes vesicles to fuse to pre-synaptic membrane (~100+ vesicles released per nerve impulse); 3. Exocytosis occurs - ACh is expelled and the vesicle becomes part of the membrane |
| Where are the Ca channels located? Voltage-gated Na channels? ACh receptors? | Ca = axon terminal; Na = bottom of subneural cleft on post-synaptic membrane; ACh = opening of subneural cleft on post-synaptic membrane |
| What is an achetylcholine(ACh) receptor? How does it work? | 1. A trans-membrane protein w/a binding site and an ion channel; 2. Two ACh molecules attach, opens the channel (it is an ACh-gated ion channel) |
| What are nicotinic ACh receptors? | Ligand-gated ion channels in the NMJ |
| What molecule inhibits the nicotinic ACh receptors? | Curare |
| What are muscarinic ACh receptors? | G-protein coupled receptors found on target organs of the sympathetic NS |
| What molecule inhibits muscarinic ACh receptors? What excites them? | Inhibit: atropine; Stimulate: pilocarpine |
| Describe the ion movement through ACh-gated ion channels | 1. Na is in high concentration in synaptic cleft; 2. K is held inside by negatively charged cytoplasm; 3. Some Ca also enters |
| What is the primary ion that depolarizes the post-synaptic muscle membrane? | Na crosses the post-synaptic membrane, enters muscle, depolarizes interior |
| What is depolarization of the post-synaptic membrane called? What is it called when this depolarization spreads? | End Plate Potential; Muscle Action Potential |
| What is the location, action, and function of acetylcholinesterase? | Location: on fibers in synaptic cleft; Action: cuts ACh into acetate ion and choline; Fxn: clears receptor for next signal |
| What is reuptake? | most of the choline is reabsorbed into the pre-synaptic membrane |
| What do reuptake-inhibitors do? | Increase the amount of NT available in the synapse |
| Describe how vesicles and ACh are made | 1. Vesicles are produced by the Golgi in neuron cell body and transported into the axon terminal; 2. ACh is synthesized in the axon terminal, then moved into the vesicles |
| Describe Clathrin | 1. Contractile protein in axon terminal; 2. After each nerve impulse, 100+ vesicles fuse w/axon terminal membrame; 3. Clathrin molecules bind to original vesicle membranes; 4. Bound clathrin contracts, forms pits --> vesicles, all inside axon terminal |
| What is Excitation-Contraction Coupling? | 1. An AP spreads across & along the sarcolemma; 2. Transverse tubules allow surface signal to access center of muscle fiber; 3. Depolarization causes Ca release from SR |
| Describe the relationship of the T-tubule (transverse tubule) and SR (see image) | Branches of T-tubules lie directly over the actin-myosin overlap, allowing Ca to be applied to the region of the myofibril that can most quickly and efficiently use it. |
| Discuss the action of DHP and Ryanodine receptors on the SR in response to Ca (see image) | 1.In skeletal muscle, DHP on sarcolemma are linked to ryanodine receptors on SR; 2.AP depolarizes interior, channels on SR open, Ca is released into cell; 3.Cell interior repolarizes, Ca channel closes, Ca pump returns Ca to the SR |
| Describe the Ca flow in contraction of cardiac muscle (see image) | Contraction: (CICR) AP opens surface Ca channels. Ca influx opens ryanodine channels on SR, which dump Ca onto the myofibrils; Relaxation: Ca pump returns Ca to SR and extracellular fluid |
| What is the action of curare? | Blocks ACh RECEPTOR. No transmission --> no contraction --> FLACCID paralysis |
| What is the action of botulism toxin? What is an example? | Blocks ACh RELEASE. No transmission --> no contraction --> FLACCID paralysis; Botox - low dose, blocks contraction |
| What is the action of neostigmine? | Inactivates ACh-esterase. ACh builds up --> spasms--> RIGID paralysis |
| What is the action of nicotine? | Strongly binds to ACh RECEPTOR. Continuous depolarization --> stimulant --> spasms |
| What is the disease process of the tetanus toxin? | Released by anaerobic Clostridium tetani. Blocks ACh release from inhibitory motor neurons --> RIGID paralysis |
| What are the Congenital Mysethenic Syndromes? What are the sx? | Mutations in ACh receptor; sx: weakness, breathing difficulty |
| What is myasthenia gravis? | An autoimmune disease - the body makes ABs to the ACh-gated channel protein |
| What are the sx of Myasthenia gravis? | No signal to muscle --> flaccid paralysis. First sxs ptosis, diplopia, dysphagia. There are cycles of flareup and remission. Involvement of respiratory muscles can be life-threatening, otherwise life expectancy is normal |
Created by:
hclark86
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