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Questions and Answers
What is the primary role of calcium in muscle contraction?
What is the primary role of calcium in muscle contraction?
- It acts as a catalyst for ATP hydrolysis during muscle contraction.
- It facilitates the attachment of actin filaments to Z disks.
- It directly initiates the conformational change in myosin.
- It causes a conformational change in the troponin complex. (correct)
How does acetylcholine influence muscle contraction?
How does acetylcholine influence muscle contraction?
- It enhances the binding of troponin to tropomyosin.
- It activates voltage-gated calcium channels directly.
- It serves as a neurotransmitter that initiates muscle action potential. (correct)
- It directly stimulates myosin ATPase activity.
Which ion channel type is primarily involved in the depolarization of the muscle fiber membrane?
Which ion channel type is primarily involved in the depolarization of the muscle fiber membrane?
- Potassium channels.
- Calcium channels.
- Chloride channels.
- Sodium channels. (correct)
What is the impact of Myasthenia Gravis on muscle function?
What is the impact of Myasthenia Gravis on muscle function?
What structural component limits the stretch of the sarcomere?
What structural component limits the stretch of the sarcomere?
What is the primary role of Acetylcholine (ACh) at the neuromuscular junction?
What is the primary role of Acetylcholine (ACh) at the neuromuscular junction?
In excitation-contraction coupling, what is the consequence of calcium (Ca²⁺) binding to troponin?
In excitation-contraction coupling, what is the consequence of calcium (Ca²⁺) binding to troponin?
Which ion is primarily responsible for the depolarization of the muscle membrane?
Which ion is primarily responsible for the depolarization of the muscle membrane?
What effect does Myasthenia Gravis have on muscle signal transmission?
What effect does Myasthenia Gravis have on muscle signal transmission?
What role do voltage-gated sodium channels play in muscle physiology?
What role do voltage-gated sodium channels play in muscle physiology?
Which component directly interacts with ryanodine receptors during the excitation-contraction coupling process?
Which component directly interacts with ryanodine receptors during the excitation-contraction coupling process?
In what way does the impairment of ACh receptors in Myasthenia Gravis manifest clinically?
In what way does the impairment of ACh receptors in Myasthenia Gravis manifest clinically?
What is the function of nicotinic acetylcholine receptors (nAChRs) at the motor endplate?
What is the function of nicotinic acetylcholine receptors (nAChRs) at the motor endplate?
How does potassium (K⁺) contribute to muscle action potentials?
How does potassium (K⁺) contribute to muscle action potentials?
Which statement correctly describes the role of calcium (Ca²⁺) in muscle contraction?
Which statement correctly describes the role of calcium (Ca²⁺) in muscle contraction?
What directly causes the exposure of myosin-binding sites on actin during muscle contraction?
What directly causes the exposure of myosin-binding sites on actin during muscle contraction?
Which statement about the roles of Ca²⁺ in muscle contraction is correct?
Which statement about the roles of Ca²⁺ in muscle contraction is correct?
In which phase does ATP bind leading to the detachment of myosin from actin?
In which phase does ATP bind leading to the detachment of myosin from actin?
What characterizes the A-band of the sarcomere during muscle contraction?
What characterizes the A-band of the sarcomere during muscle contraction?
What is the correct order of the cross-bridge cycle steps?
What is the correct order of the cross-bridge cycle steps?
How does myasthenia gravis affect muscle contraction?
How does myasthenia gravis affect muscle contraction?
Which structure defines the boundary of the sarcomere?
Which structure defines the boundary of the sarcomere?
What occurs to the I-band during muscle contraction?
What occurs to the I-band during muscle contraction?
Which component of the sarcomere covers actin's myosin-binding sites when the muscle is at rest?
Which component of the sarcomere covers actin's myosin-binding sites when the muscle is at rest?
What is primarily responsible for the power stroke during contraction?
What is primarily responsible for the power stroke during contraction?
What is the primary role of dystrophin in muscle cells?
What is the primary role of dystrophin in muscle cells?
In the context of excitation-contraction coupling, what triggers the release of Ca²⁺ from the sarcoplasmic reticulum?
In the context of excitation-contraction coupling, what triggers the release of Ca²⁺ from the sarcoplasmic reticulum?
What is the effect of myasthenia gravis on neuromuscular transmission?
What is the effect of myasthenia gravis on neuromuscular transmission?
Which ion is primarily responsible for depolarization during excitation at the neuromuscular junction?
Which ion is primarily responsible for depolarization during excitation at the neuromuscular junction?
What compensatory mechanism occurs in muscle cells to restore Ca²⁺ levels during repolarization?
What compensatory mechanism occurs in muscle cells to restore Ca²⁺ levels during repolarization?
Which component is primarily involved in the release of acetylcholine at the neuromuscular junction?
Which component is primarily involved in the release of acetylcholine at the neuromuscular junction?
How does the presence of high levels of magnesium in sarcoplasm affect muscle contractions?
How does the presence of high levels of magnesium in sarcoplasm affect muscle contractions?
What aspect of neuromuscular junction physiology is primarily affected in Duchenne muscular dystrophy?
What aspect of neuromuscular junction physiology is primarily affected in Duchenne muscular dystrophy?
What role do terminal cisternae play in skeletal muscle physiology?
What role do terminal cisternae play in skeletal muscle physiology?
What initiating event occurs at the motor endplate of a muscle cell that leads to muscle contraction?
What initiating event occurs at the motor endplate of a muscle cell that leads to muscle contraction?
What is the primary function of T-tubules in muscle fibers?
What is the primary function of T-tubules in muscle fibers?
How do dihydropyridine receptors (DHPR) contribute to muscle contraction?
How do dihydropyridine receptors (DHPR) contribute to muscle contraction?
What initiates the exposure of myosin-binding sites on actin filaments during muscle contraction?
What initiates the exposure of myosin-binding sites on actin filaments during muscle contraction?
Which subunit of the troponin complex directly binds calcium ions?
Which subunit of the troponin complex directly binds calcium ions?
What role does tropomyosin play in muscle contraction?
What role does tropomyosin play in muscle contraction?
In the context of excitation-contraction coupling, what is the function of the sarcoplasmic reticulum (SR)?
In the context of excitation-contraction coupling, what is the function of the sarcoplasmic reticulum (SR)?
What is the impact of myasthenia gravis on muscle contraction?
What is the impact of myasthenia gravis on muscle contraction?
What process occurs after calcium ions bind to troponin C during muscle contraction?
What process occurs after calcium ions bind to troponin C during muscle contraction?
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Study Notes
T-Tubules and Muscle Contraction
- T-tubules are invaginations of the sarcolemma that transmit action potentials deep into muscle fibers, promoting synchronized contraction.
Dihydropyridine Receptors (DHPR) and Ryanodine Receptors (RyR)
- DHPRs are voltage-sensitive receptors on T-tubules that detect action potentials, leading to a conformational change.
- RyRs are channels on the sarcoplasmic reticulum that release calcium ions (Ca²⁺) into the cytosol when activated by DHPRs.
Calcium Ions (Ca²⁺) in Muscle Contraction
- Released Ca²⁺ binds to troponin C, initiating the cross-bridge cycle by exposing myosin-binding sites on actin.
Troponin Complex
- Composed of three subunits:
- Troponin C (TnC) binds Ca²⁺, triggering conformational changes.
- Troponin I (TnI) inhibits actin-myosin interaction in the absence of Ca²⁺.
- Troponin T (TnT) anchors to tropomyosin, aiding in contraction regulation.
- Ca²⁺ binding to TnC shifts tropomyosin away from actin binding sites, allowing myosin interaction.
Tropomyosin
- A regulatory protein that blocks myosin-binding sites on actin when the muscle is relaxed, preventing contraction.
Myosin
- A motor protein that binds to actin filaments, generating force through the cross-bridge cycle with ATP.
Sarcoplasmic Reticulum (SR) Functions
- The SR is the intracellular store of Ca²⁺, which is pumped back by the SERCA pump during relaxation to end contraction.
Cross-Bridge Cycling Process
- The cycle, essential for muscle contraction, occurs in several stages:
- Resting State: Myosin heads are energized; tropomyosin covers actin binding sites.
- Calcium Release: Ca²⁺ binds to TnC, exposing myosin-binding sites.
- Cross-Bridge Formation: Myosin head attaches to actin.
- Power Stroke: Myosin head pivots, pulling actin closer to the sarcomere center.
- Cross-Bridge Detachment: Binding of ATP to myosin head causes detachment.
- Reactivation of Myosin: ATP hydrolysis re-cocks the myosin head for another cycle.
Sarcomere Structure
- Key components include:
- Z-line: Boundary defining the sarcomere.
- Actin: Thin filaments anchored to the Z-line.
- Myosin: Thick filaments in the center.
- Tropomyosin and Troponin: Regulate actin-myosin interactions.
- During contraction, Z-lines move closer, I-band shortens, H-zone disappears, and A-band remains constant.
Preload Principle
- Preload refers to the initial stretching of the muscle before contraction, affecting sarcomere length and subsequent contractile force.
Dystrophin and Sarcoplasm
- Dystrophin anchors thin and thick filaments to the cytoskeleton, aligning Z-disks with adjacent myofibrils.
- Sarcoplasm contains high levels of Mg²⁺, phosphates, and myoglobin, with abundant mitochondria for ATP production.
Key Players in Excitation-Contraction Coupling
- Acetylcholine (ACh): Neurotransmitter initiating depolarization at the neuromuscular junction (NMJ).
- Nicotinic ACh Receptors (nAChRs): Ligand-gated channels that open upon ACh binding, allowing Na⁺ influx.
- Sodium Ions (Na⁺): Primary drivers of depolarization in muscle fibers.
- Voltage-Gated Sodium Channels: Amplify depolarization to propagate action potentials.
Neuromuscular Junction (NMJ) Steps
- Action potential reaches motor neuron terminal.
- Ca²⁺ influx triggers ACh release into the synaptic cleft.
- ACh binds to nAChRs, causing Na⁺ influx and sarcolemma depolarization.
- Action potential travels down T-tubules, activating DHPR and RyR, leading to Ca²⁺ release and muscle contraction.
Clinical Correlations
- Duchenne Muscular Dystrophy: Caused by dysfunction of dystrophin, leading to muscle fiber necrosis and wasting.
- Myasthenia Gravis: An autoimmune disorder that attacks ACh receptors at the NMJ, resulting in muscle weakness and fatigue.
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