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Question 1: Explain how a stimulus voltage applied to the gastrocnemius muscle caused its’ contraction (ie, how does the stimulus activate the muscle cells – ie how is an action potential generated). How can the force of contraction be elevated by increases in voltage applied to the muscle (include a discussion of motor unit recruitment)?

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Beverley Smith
Beverley SmithLv2
28 Sep 2019
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Related questions

3. a) The neurotransmitter that is responsible for “communication” 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)

receptor

Agonist

antagonist

a1

Norephinephrine

Phenylephrine

a2

Phenoxybenzamine

Prazosin

B1

Clonidine

Yohimbine

Norephinephrine

Propranolol

Epinephrine

Metoprolol

Isoproterenol

Dobutamine

B2

Epinephrine

Proranolol

Norepinephrine

Butoxamine

Isoproterenol

Albuterol

Nicotinic

Ach

Curare

Nicotine

Hexamethonium

Muscarinic

Ach

Atropine

Assume all the chemicals in the table are available to you.

You are given a piece of smooth muscle tissue, you stimulate it with Norepinephrine and find the muscle responds with contractions. Your hypothesis is that the muscle contraction is caused by the activation of α1 adrenergic receptors. Now you need to design an experiment protocol to test your hypothesis.

Background knowledge: The figure below is an experiment setup, the red tissue in the organ bath is the smooth muscle tissues. In this kind of experiment smooth muscle tissue is minimally stretched vertically by two hooks or clips in the organ bath filled with physiological saline solution (PSS). Agonist is added to the PSS to challenge the muscle tissue, muscle contraction is sensed by a force transducer at the top and force is recorded by a computer. Adding antagonist before adding agonist blocks agonist action. PSS may or may not be changed, it depends on your purposes, e.g. if you want to block a type receptors, then you do not want change PSS after you add antagonist to the PSS. Your correct step is that you add antagonist to PSS, wait some time, and add agonist, you keep both antagonist and agonist in the PSS so that you can judge if the receptor blockage by antagonist abolish the agonist action.

The key to this assignment is that you eliminate possible cross-activities of agonists. Cross-activity means an agonist activate more than one types of receptors, you need block each type of the receptor in order to see what type of the receptor is activate to cause contraction. This muscle tissue can have both α and β receptor types and their subtypes, you need to demonstrate convincingly that you only stimulate α1 receptors.

Write an experimental protocol to demonstrate your work, for each step in the protocol you write the chemical(s) you add, why you add, what result you are expecting to see e.g. contract, relax, no response. If the step is to wash the tissue with fresh PSS, then you do not need to indicate the responses.

Here is an example of the answer.

step

chemical added

response

1.

epinephrine, activate alpha and beta receptors,

blood vessel ring contract slightly.

2.

wash with PSS

3.

alpha receptor antagonist and norepinerphine, block NE activating alpha receptor.

blood vessel ring should not contract.

4.

wash with PSS

5.

…

…

6.

…

…

Discuss your protocol to show the relation between activation of α1 receptors and the vascular smooth muscle contraction.Design the experiemnt and its conclusion/ results.

1. Each muscle fiber is a bundle of myofibrils. Eachmyofibril is a series of sarcomeres. Thus, a muscle fiber contractswhen each sarcomere within a series contracts simultaneously. Suchcoincidence is mirrored by each myobril within the muscle fiber.What enables the extent to which molecular motors contractsimultaneously within an innervated muscle fiber?

a. the frequency of acetylcholine secretion within theneuromuscular synapse

b. the frequency of Ca2+ oscillations within themuscle fiber

2. A living muscle fiber experiences dynamic frequencies ofCa2+ oscillations. In effect, Ca2+ acts as asecond messenger when it disperses throughout the fluid-filledspaces between actin and myosin filaments. What is the source ofthis second message?

a. extracellular fluid b.sarcoplasmic reticulum

3. Why might a muscle fiber need an ample amount ofNa+,K+-ATPase on itssurface?

a. as evident by the value of the cell’s membrane potential,muscle fibers are leaky to Na+

b. to counter the effect of numerous action potentials persecond

4. Assume that you could “see” nicotinic acetylcholine receptorswithin the musculature. How would they be arranged spatially?

a. evenly distributed on the cell’s surface like voltage-gatedNa+ and K+ channels

b. in dense arrays within the motor end plate

5. Assume that you could “see” neurosecretion fromα-motor neurons within the musculature of an animal standing still.What would this “look” like?

a. uniform, baseline secretion throughout the musculature

b. enhanced acetylcholine secretion within antigravity muscles,baseline secretion elsewhere

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