BIOL 22000 Lecture Notes - Lecture 11: Sodium Channel, Sarcomere, Cisterna

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26 Jun 2018

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Lecture 11

Outline – excitation-contraction coupling

oAnatomy of Skeletal Muscle

oExcitation – synaptic transmission at the neuromuscular junction

oCoupling – release of intracellular calcium

oContraction – sliding filament theory



oBoth skeletal muscle and cardiac muscles are striated muscle

oA unique characteristic is that skeletal muscles is that fiber cell is large

oCardiac cells are smaller and are not polynucleated

Anatomy of Skeletal Muscle

oMuscle cells are called muscle fibers

Fused cells with many nuclei

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Cells bundled into fascicles sorrunded by connective tissue

oFiber internal structures

Sarcolemma: cell membrane

Sarcoplasm: cytoplasm

Sarcoplasmic reticulum: endoplasmic reticulum

Network of transverse tubules: T-tubules connected with the sarcolemma

This allows plasma membrane to go all the way through the inside

of the muscle cells

Because the plasma membrane can generate action potential, the

action potential can conduct all the way to the inside of the muscle

cell, and bring the excitation all the way in the center of the muscle

fiber

oMyofibrils are the contractile structures

Actin: thin filament

Myosin: thick filament

Accessory proteins: troponin and tropomyosin

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

oThe nerve is the axon that is coming down to control the muscle fiber

Structure of a Skeletal muscle Fiber

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Document Summary

Anatomy of skeletal muscle: muscle cells are called muscle fibers. Cells bundled into fascicles sorrunded by connective tissue: fiber internal structures. Network of transverse tubules: t-tubules connected with the sarcolemma. This allows plasma membrane to go all the way through the inside of the muscle cells. Accessory proteins: troponin and tropomyosin: the nerve is the axon that is coming down to control the muscle fiber. T-tubules are just sarcolemma embedded in the muscle cells. When there is an action potential, it propagates down the t-tubule and go all the way inside. Sarcoplasmic reticulum is the calcium storage in muscle cells. When muscle cells are excited, sarcoplasmic reticulum release calcium right on top of myofibril. Myosin head bind atp, so they are atpase. Myosin head has binding site for actin: actin has two forms. G-actin molecule each individual represent globule actin, also bind site.

Related Questions

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

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BIOL 22000 Lecture Notes - Lecture 11: Sodium Channel, Sarcomere, Cisterna

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