BIOL 2443 Lecture 8: L18

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whiteimpala998

20 Feb 2019

School

University of Arkansas

Department

Biology

Course

BIOL 2443

Professor

Dr.Vo

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Document Summary

Block 2: acetylcholine or ach, travels across the synaptic cleft, binds to membrane receptors on sarcolemma (motor end plate, causes sodium ion rush into sarcoplasm. Adp+pi (power stroke: myosin binds atp, releasing actin, myosin recocks using the energy from atp, hydrolyzing it to adp+pi (energized state) Ach release na+ channel activation . Block 2 bridge formation power stroke myosin reset/repeat . Contraction: neural stimulation of sarcolemma, causes excitation contraction coupling, cisternae of sr release ca2+, which triggers interaction of thick and thin filaments, consuming atp and producing tension. Ion pumps cease to function; ran out of atp: calcium builds up in the sarcoplasm. Block 2: myosin binds actin and contracts but cannot release (no more. Size of muscle and size of mvmt affect potential to reach peak of tension production: tension produced by whole skeletal muscles, depends on. Block 2: tension produced by whole skeletal muscles, recruitment (multiple motor unit summation)

Related Questions

1.If the supply of ATP to a shortening muscle is completelydepleted, what will happen to the cross-bridge cycle? What is thename if the phenomenon that results from complet ATP depletion?

2.Order the following 10 events that summarize musclecontraction. Remember that a muscle contraction begins with thetransmission of a nerve impulse to a muscle fiber

a. the power stroke

b. Opening of ryanodine Ca2+ channels in the sarcoplasmicreticulum

c. Binding of mysosin cross-bridges to actin

d. release of acetylcholine into the neuromuscular junction

e. confromational change in tropomyosin troponin complex

f. binding of ca2+ to troponin

g. binding of atp to myosin cross-brisges

h. depolarization of the muscle fiber

i. hydrolysis of atp bound to myosin cross-bridges

j. action potential propagation along the transverse tubules

pearpig306

Instructions: Select 2 potential antidotes only from those listed in the box at the bottom.

More than 2 correct answers are possible. For credit you must submit this in class on TUES., Feb. 21 See the 2 sample answers for atropine & physostigmine.

POISON Mode of Action ANTIDOTE

Select 2 from those listed in the box below!

Atropine blocks neurotransmitter (2), (6)

(from belladonna) acetylcholine binding to

post-synaptic receptors

Nicotine mimics the action of acetylcholine

(from tobacco) in NMJ

Physostigmine inhibitor of acetylcholinesterase (4), (5)

(in calabar bean) (in NMJ)

Botulinum Toxin [Botox] blocks vesicles from releasing

(causes botulism) acetylcholine into NMJ

Digoxin inhibitor of Na⁺/K⁺ ATPase

(cardiac medication) pump in axon membrane

Black widow venom enhances release of acetylcholine into NMJ

(latrotoxin) by synaptic vesicles

Pufferfish toxin blocks closed Na⁺ gates of axon

(tetrodotoxin)

NMJ = neuromuscular junction (synapse between neuron & muscle cell)

POTENTIAL ANTIDOTES:

(1) atropine; (2) nicotine; (3) physostigmine; (4) botulinum toxin;

(5) digoxin; (6) black widow venom; (7) pufferfish toxin

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 2443 Lecture 8: L18

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