BIOB34H3 Lecture Notes - Lecture 16: Atp Hydrolysis, Conformational Change, University Of Manchester

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4 Oct 2016

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The neuromuscular junction is the synaptic connection between a motor nerve and a skeletal muscle. Nerves that regulate skeletal muscle function are called motor nerves. When an action potential arrives at the nerve (axon) terminal, it causes the release of the neurotransmitter acetylcholine (ach). Acetylcholine then binds to an acetylcholine receptor on the post-synaptic membrane (i. e. , the muscle cell membrane; called the sarcolemma). In this case, the ach receptor is a nicotinic acetylcholine receptor (or simply a nicotinic receptor) because it is also activated by nicotine. The nicotinic receptor is a na+ channel and the binding of ach to the receptor opens the channel and na+ enters the muscle cell, depolarises it and triggers an action potential in the muscle cell: skeletal muscle structure. They are very long, multi-nucleated cells that are packaged, with connective tissue, into bundles called fascicles. In turn, the whole muscle consists of multiple fascicles surrounded by layers of connective tissue.

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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

3. a) The neurotransmitter that is responsible for âcommunicationâ at the neuromuscular junction between motor nerve cells and skeletal muscle fibers is acetylcholine (ACh). The ACh receptor protein is a channel that opens when ACh binds. Upon the opening of this channel, the membrane at the motor end plate region of the muscle cell becomes depolarized, resulting in the generation of an action potential in the muscle fiber membrane. The ACh receptor channel is equally permeable to both Na⁺ and K⁺ ions. Explain how opening a channel that allows both potassium and sodium to cross the membrane results in membrane depolarization. (2 points)

b) In normal individuals, a single end-plate potential (EPP) is always sufficient to elicit an action potential (and hence contraction) in a skeletal-muscle fiber. This is not the case in individuals suffering from myasthenia gravis (MG). MG is an autoimmune disorder in which antibodies are produced that attack the AChRs at skeletal-muscle endplates reducing their number. Patients suffering from the disease present with significant muscle weakness. Explain why patients with MG would exhibit muscle weakness. (2 points)

c) Treatment strategies for myasthenia gravis include thymectomy (removing the source of the antibody producing cells) or immunosuppressant drug therapy (inhibiting the synthesis and release of the antibodies). In addition, the drug neostigmine administered at carefully monitored doses is highly effective in treating myasthenia gravis. Investigate the actions of neostigmine, and discuss in detail why it may be an effective treatment. (2 points)

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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BIOB34H3 Lecture Notes - Lecture 16: Atp Hydrolysis, Conformational Change, University Of Manchester

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