excitation of skeletal muscles

Question 1

neuromuscular junction

Answer 1

physical place where a nerve ending and muscle fiber meet

Question 2

secretion of acetylcholine (4)

Answer 2

1. small vesicles are formed by golgi apparatus and transported to NMJ - about 300,000 collect at NMJ
2. Ach is synthesized in cytosol and transported into vesicles. about 10,000 molecules of Ach
3. when AP reached terminal, charge becomes (-) so Ca channels (next to dense bars) increase concentration inside cell (b/c Ca gets close to cell) 4. this causes vesicles to fuse with membrane and burst- which releases Ach into synaptic space

Question 3

effect of Ach on postsynaptic space (3)

Answer 3

1. once ach is in synaptic cleft, it binds with ACh-gated ion channels located on muscle membrane (immediately below dense bars)
2. 2 ach molecules are required to open 1 channel
3. once the acho-gated channel opens massive amts of Na enters muscle fiber (k and Ca can also pass)

Question 4

breakdown of acetycohline (3)

Answer 4

1. ach is destoryed by acetylcholineesterase (into acetate and choline)
2. acetate diffuses back into molecule and enters Krebs cycle for energy
3. choline is reabsorbed by axon terminal and helps with endocytosis

Question 5

myasthenia gravis

Answer 5

autoimmune disease in which patients developed antibodies to their own ach-ion channels. paralysis occurs because can’t transmit signals from nerve to muscle fibers. patient can die of paralysis of respiratory muscles

Question 6

muscle vs. nerve action potential (4)

Answer 6

1. resting potential = -80–90mV (similar)
2. duration of AP 1-5 miliseconds in skeletal muscle = 5x longer than large mylenated fibers
3. velosicty of conduct = 3-5s in skeletal muscle, 1/8 velocity conduction in large myelinated nerve fibers
4. muscle fibers are so big they use excitation-contraction coupling to transmit signals all the way into the muscle fiber

Question 7

excitation- contraction coupling (4)

Answer 7

1. t-tubles are internal extensions of cell membrane, located close to myofibrils and SR
2. facilitate contraction by providing faster pathway for AP to reach and stimulate SR (which is what releases Ca to bind to tropononin-C and start myosin cross bridging)
3. excitatory pulse = full excitation of t-tuble and SR cause 500 fold increase in myofibrilar fluid which is 10x more than enough needed for maximum contraction
4. Ca released in cytoplasm is quickly pumped back into SR by Ca pump and muscle contraction stops.