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The nerve impulse that initiates muscular contraction A. begins with binding of acetylcholine to receptors in the sarcoplasmic reticulum. B. causes both plasma membrane and transverse tubules to undergo hyperpolarization. C. causes opening of calcium channels, leading to an increase in \(\mathrm{Ca}^{2+}\) within the sarcomere. D. prevents \(\mathrm{Na}^{+}\) from entering the sarcomere. E. prevents \(\mathrm{Ca}^{+2}\) from binding to troponin \(\mathrm{C}\)

Short Answer

Expert verified
Answer: (C) The nerve impulse that initiates muscular contraction causes opening of calcium channels, leading to an increase in Ca^2+ within the sarcomere.

Step by step solution

01

Overview of Muscle Contraction

Muscle contraction is a complex process that requires the interaction of several components, including nerve impulses, neurotransmitters, ions, and proteins within muscle cells. The mechanism is known as the sliding filament theory, where myosin filaments slide along actin filaments, causing contraction of the muscle.
02

Role of Acetylcholine in Muscle Contraction

Acetylcholine is a neurotransmitter that is released at the neuromuscular junction by a motor neuron. It binds to receptors on the muscle cell membrane, known as the sarcolemma. This binding leads to the generation of an electrical signal (action potential) that travels along the sarcolemma and enters the muscle cell through the transverse (T) tubules.
03

Role of Calcium Ions in Muscle Contraction

The action potential from the T tubules causes the release of calcium ions (\mathrm{Ca}^{2+}) from the sarcoplasmic reticulum into the cytoplasm of the muscle cell. The increased concentration of \mathrm{Ca}^{2+} ions leads to their binding to troponin C, a regulatory protein on the actin filament. This binding results in a conformational change in the troponin complex, causing the tropomyosin to move and uncover the binding sites for myosin on the actin filament. This enables the interaction of myosin and actin filaments, leading to muscle contraction.
04

Evaluation of the Statements

Now let's evaluate each statement: A. Acetylcholine binds to receptors on the sarcolemma (not sarcoplasmic reticulum), so this statement is incorrect. B. The action potential causes depolarization (not hyperpolarization) of the plasma membrane and T tubules, so this statement is incorrect. C. The action potential causes the opening of calcium channels in the sarcoplasmic reticulum, leading to an increase in \mathrm{Ca}^{2+} within the sarcomere. This statement is correct. D. The action potential causes depolarization, leading to an influx of \mathrm{Na}^{+} ions (not preventing their entry), so this statement is incorrect. E. The increase in \mathrm{Ca}^{2+} ions leads to their binding to troponin C (not preventing their binding), so this statement is incorrect.
05

Conclusion

Based on the analysis of each statement, the correct answer is (C): The nerve impulse that initiates muscular contraction causes opening of calcium channels, leading to an increase in \mathrm{Ca}^{2+}$ within the sarcomere.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Role of Acetylcholine in Muscle Contraction
Understanding how muscles contract begins at the intersection of the nervous system and the muscular system—the neuromuscular junction. Here, acetylcholine plays a pivotal role as the chemical messenger. When an electrical nerve impulse, or action potential, reaches the end of a motor neuron, acetylcholine is released into the synaptic cleft. This neurotransmitter then binds to specific receptors on the muscle cell's outer membrane, known as the sarcolemma.

This binding action is the key that unlocks muscle contraction. It triggers an electrical impulse in the muscle cell that leads to a series of events culminating in muscle contraction. It's like flipping a light switch; the presence of acetylcholine 'turns on' the muscle's contraction machinery. Without acetylcholine, the muscle remains in its resting state, akin to a car that won't start without the turn of its ignition key.

Therefore, it's inaccurate to suggest that acetylcholine binds to receptors in the sarcoplasmic reticulum, as its true point of action is on the sarcolemma. The latter's subsequent depolarization is what stimulates muscle contraction—a fundamental understanding for any student of biology or medicine.
Calcium Ions in Muscle Contraction
Once the electrical impulse is initiated by acetylcholine, it paves the way for calcium ions (Ca2+) to take center stage. These ions are sequestered within the sarcoplasmic reticulum, a specialized form of endoplasmic reticulum in muscle cells. The wave of depolarization caused by acetylcholine influences the sarcoplasmic reticulum to release these stored Ca2+ ions into the cytoplasm of the muscle cell.

This surge in Ca2+ concentrations sets off a critical chain reaction by interacting with the troponin complex on the actin filaments. Here, they bind to troponin C, leading to a shift in the troponin-tropomyosin complex that unveils myosin-binding sites on the actin strands. It's as if the calcium ions play a musical note that cues the proteins to dance—a sequence of precise movements enabling contraction. This Ca2+ ion-troponin interaction is instrumental, and without it, the muscle fibers would remain in their elongated, relaxed state. The exercise's correct answer reflects this principle by acknowledging the crucial role calcium plays in this biological symphony.
Sliding Filament Theory
To visualize muscle contraction, the sliding filament theory offers an excellent framework. This model suggests that muscle fibers shorten during contraction because the thin (actin) and thick (myosin) filaments slide past one another without actually shortening themselves. Picture two sets of interlocked combs being pulled in opposite directions; the teeth symbolize the overlapping actin and myosin filaments.

Once the Ca2+ ions have exposed the binding sites on actin and the ATPase activity on myosin heads is activated, the myosin heads rotate and pull on the actin filaments. This ratcheting action is much like rowing a boat; the oars (myosin) pull against the water (actin) to propel you forward. The result is that the Z-lines, to which actin filaments are attached, move closer together, shortening the sarcomere—the fundamental unit of muscle contraction. This beautiful mechanism embodies a complex biological process we often take for granted, from performing high-speed sprints to simply blinking an eye.

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Most popular questions from this chapter

When a muscle contracts, the A. transverse tubules shorten, drawing the myofibrils and sarcoplasmic reticulum closer. B. thin filaments and thick filaments of the sarcomere shorten. C. light chains dissociate from the heavy chains of myosin. D. \(\mathrm{H}\) bands and I bands of the sarcomere shorten because thin filaments and thick filaments slide past each other. E. cross-linking of proteins in the heavy filaments increases.

In the presence of warfarin, an analog of vitamin \(\mathrm{K}\), several proteins of the blood coagulation pathway are ineffective because they cannot bind \(\mathrm{Ca}^{2+}\) efficiently. Why?

The cye relies heavily on the metabolism of glucose but different parts of the eye use glucose differently. Which of the following statements is/are correct? A. The retina uses glucose primarily by aerobic glycolysis and the TCA cycle. B. The cornea uses over half its glucose via the hexose monophosphate pathway. C. The lens has the glycolytic pathway but not the hexose monophosphate pathway. D. The role of glutathione reductase is to inactivate active oxygen species. E. All of the above.

All of the following statements about actin and myosin are true except A. the globular head section of myosin has domains for binding ATP and actin. B. actin is the major protcin of the thick filament. C. binding of ATP to the actin-myosin complex promotes dissociation of actin and myosin. D. F-actin is stabilized when tropomyosin is bound to it. E. binding of \(\mathrm{Ca}^{2+}\) to the calmodulin-like subunit of troponin induces conformational changes that permit myosin to bind to actin.

Lysis of a fibrin clot A. is in equilibrium with formation of the clot. B. begins when plasmin binds to the clot. C. requires the hydrolysis of plasminogen into heavy and light chains. D. is regulated by the action of protein inhibitors on plasminogen. E. requires the conversion of plasminogen to plasmin by t-PA.

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