Exam 3 Flashcards
Describe briefly the steps of a contraction cycle
Calcium binds to troponin causing a conformational change which moves tropomyosin off of the myosin binding site
1) Myosin head hydrolized ATP and becoms energized and oriented.
2) Myosin head binds to actin forming a cross-bridge
3) Myosin head pivots, pulling the thin filaments past the thick filament toward center of the sarcomere
4) As myosin head binds ATP the cross-bridge detaches from actin
When does the muscle fiber start to relax?
As Ca++ ion is pumped back to sarcoplasmic reticulum, Ca++ is no longer bound to troponin causing tropomyosin molecules to block the myosin binding site on actin. This prevents the interaction between actin and myosin head and muscles start to relax.
What is a sarcomere
Sarcomere is the contractile unit in myofibril defined by the part of a myofibril between two consecutive Z-disc.
What are the functions of actin
Contractile protein that is the main component af thin filament; each actin molecule has a myosin binding site where myosin head of thick filament binds during muscle contraction
What are the functions of myosin
Contractile protein that makes up thick filement; molecules consists of a tail and two myosin heads which bind to myosin-binding sites on actin molecules of thin filament during muscle contraction
What are the functions of titin
Structural protein that connects Z-discs to M-line of sarcomere thereby helping to stabilize thick filament position, can strech and then spring back unharmed and thus accounts for much of the elastcity and extensibility of myofibrils
How does the protein dystrophin help in the contraction of muscle fibers?
Dystrophin is a rod-shaped protein that connects the ends of myofibrils (from Z-disc) to a protein complex containing dystroglycan in sarcolemma (plasma membrane). Dystroglycan provides attachment to extracellular matrix protein laminin and is essential for transmitting individual myofibril-generated force to connective tissue.
What disease condition can result from a mutation in the dystrophin gene resulting in defective protein synthesis?
Duchenne muscular dystrophy can result from a mutation in the dystrophin gene
-Weakness of muscular mass
What is the effect of calcium entry in the synaptic end bulbs following an action potential?
Calcium entry in the synaptic end bulbs causes exocytosis of Ach containing synaptic vesicles in the synaptic cleft
See figur 10.9
Give examples of two molecules that block the transmission at the neuromuscular junction by separate mechanisms.
Molecules blocking synaptic transmission:
- Botulinum toxin
- Curare
Weightlifter Jamal has been practicing many hours a day and his muscles have gotten noticeably bigger. He tells you that his muscle cells are “multiplying like crazy and making him get stronger and stronger.” Do you believe his explanation? Why or why not
No, because mature skeletal muscle fibers generally does not undergo mitosis
What is the muscle hypertrophy
Hypertrophy (Increase in the muscle mass): (a) increase in actin and myosin filaments in each myofibril and (b) splitting of myofibril. Hypertrophy occurs to a much greater extent when the muscle is loaded during the contractile process. The enzyme systems that provide energy (especially enzymes for glycolysis) also increases
What is muscle hyperplasia
Hyperplasia (increase in the number of muscle fibers): Very rarely, under intense condition skeletal muscle fibers are observed to divide.
Find in the smooth muscle
What is atrophy
Atrophy: Muscle mass decreases over time; here the degradation of the contractile proteins is more rapid than the rate of replacement.
Write any three differences observed between the structures of skeletal and cardiac muscle tissue.
Major difference from skeletal muscle:
- Single nucleus
- Intercalated discs (gap junctions and desmosomes)
- Functions as a syncytium
- Autorhythmic
- Prolonged duration of action potential (200-300 ms as -opposed to 1-2 ms in skeletal muscles
Why cardiac muscle fibers have a more prolonged action potential compared to skeletal muscle fibers?
Why duration of action potential is cardiac muscles is much longer:
- Opening of slow Ca++ channel follows the opening of fast Na+ channels
- Inhibition of Ca++ dependent K+ channel prevents outwards K+ flux.
Smooth muscle fibers lack striations; does this suggest that smooth muscle cells lack actin and myosin filaments?
Even striations are absent, actin and myosin are highly organized in smooth muscle.