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Questions and Answers
In the context of sarcomere structure and function, what is the consequence of a mutation that disrupts the lattice-like arrangement of titin filaments within the I-band?
In the context of sarcomere structure and function, what is the consequence of a mutation that disrupts the lattice-like arrangement of titin filaments within the I-band?
- Accelerated degradation of myosin filaments, leading to decreased force generation.
- Impaired transmission of action potentials along the T-tubules, resulting in asynchronous muscle contraction.
- Disrupted calcium ion sequestration within the sarcoplasmic reticulum, leading to sustained muscle contraction.
- Compromised structural integrity and elasticity, causing increased susceptibility to over-stretching and muscle damage. (correct)
If a novel competitive inhibitor selectively binds to the ATP hydrolysis site on myosin, but does not prevent ATP binding, what is the most likely immediate effect on cross-bridge cycling?
If a novel competitive inhibitor selectively binds to the ATP hydrolysis site on myosin, but does not prevent ATP binding, what is the most likely immediate effect on cross-bridge cycling?
- Myosin remains tightly bound to actin, preventing detachment and muscle relaxation. (correct)
- Calcium binding to troponin is inhibited, preventing the exposure of myosin-binding sites on actin.
- The power stroke is enhanced, leading to increased force production.
- Cross-bridge formation is inhibited due to the inability of myosin to bind to actin.
Consider a scenario where a genetically modified muscle fiber expresses a constitutively active form of calsequestrin within the sarcoplasmic reticulum (SR). This modification leads to a significant increase in the SR's calcium-buffering capacity. What is the most likely effect on muscle contraction?
Consider a scenario where a genetically modified muscle fiber expresses a constitutively active form of calsequestrin within the sarcoplasmic reticulum (SR). This modification leads to a significant increase in the SR's calcium-buffering capacity. What is the most likely effect on muscle contraction?
- Increased amplitude and duration of muscle contraction due to enhanced calcium release.
- Sustained muscle contraction due to impaired calcium re-uptake.
- Decreased calcium sensitivity of troponin, resulting in weakened muscle contraction. (correct)
- Enhanced re-uptake of calcium into the SR, causing rapid muscle fatigue.
In a hypothetical experiment, researchers selectively modify the acetylcholine receptors (AChRs) at the neuromuscular junction (NMJ) of a skeletal muscle fiber. These modified AChRs exhibit a significantly prolonged open time upon binding to acetylcholine (ACh). Which of the following physiological effects is most likely to occur as a direct result of this modification?
In a hypothetical experiment, researchers selectively modify the acetylcholine receptors (AChRs) at the neuromuscular junction (NMJ) of a skeletal muscle fiber. These modified AChRs exhibit a significantly prolonged open time upon binding to acetylcholine (ACh). Which of the following physiological effects is most likely to occur as a direct result of this modification?
Certain snake venoms contain toxins that irreversibly block voltage-gated sodium channels. If such a venom were introduced locally to a muscle, what immediate effect would be observed at the neuromuscular junction following nerve stimulation?
Certain snake venoms contain toxins that irreversibly block voltage-gated sodium channels. If such a venom were introduced locally to a muscle, what immediate effect would be observed at the neuromuscular junction following nerve stimulation?
Consider an experiment where a non-hydrolyzable analog of GTP is introduced into the presynaptic terminal at the neuromuscular junction. How would this most likely affect the release of acetylcholine (ACh)?
Consider an experiment where a non-hydrolyzable analog of GTP is introduced into the presynaptic terminal at the neuromuscular junction. How would this most likely affect the release of acetylcholine (ACh)?
If a mutation caused a loss of function of acetylcholinesterase, what downstream effect would be expected at the neuromuscular junction?
If a mutation caused a loss of function of acetylcholinesterase, what downstream effect would be expected at the neuromuscular junction?
A researcher discovers a novel toxin that selectively inhibits the function of dihydropyridine receptors (DHPRs) in skeletal muscle cells. Which of the following downstream events would be most directly affected by this toxin?
A researcher discovers a novel toxin that selectively inhibits the function of dihydropyridine receptors (DHPRs) in skeletal muscle cells. Which of the following downstream events would be most directly affected by this toxin?
Consider a mutation that results in a loss of the M-line proteins within a sarcomere. What effect would this have on muscle contraction?
Consider a mutation that results in a loss of the M-line proteins within a sarcomere. What effect would this have on muscle contraction?
Imagine introducing a high concentration of a non-selective phosphatase into the cytoplasm of a muscle fiber that is actively contracting. What direct effect would this have on the cross-bridge cycle?
Imagine introducing a high concentration of a non-selective phosphatase into the cytoplasm of a muscle fiber that is actively contracting. What direct effect would this have on the cross-bridge cycle?
A novel drug is developed that selectively prevents the binding of calcium ions to troponin. What direct effect would this drug have on skeletal muscle contraction?
A novel drug is developed that selectively prevents the binding of calcium ions to troponin. What direct effect would this drug have on skeletal muscle contraction?
If a researcher were to selectively remove titin from a muscle fiber, what would be the immediate consequence on the fiber's mechanical properties?
If a researcher were to selectively remove titin from a muscle fiber, what would be the immediate consequence on the fiber's mechanical properties?
In malignant hyperthermia, a mutation in the ryanodine receptor (RyR1) causes uncontrolled release of calcium from the sarcoplasmic reticulum. Which of the following interventions would be most directly effective in counteracting the effects of this condition?
In malignant hyperthermia, a mutation in the ryanodine receptor (RyR1) causes uncontrolled release of calcium from the sarcoplasmic reticulum. Which of the following interventions would be most directly effective in counteracting the effects of this condition?
A researcher engineers a muscle fiber to express a mutant form of tropomyosin that permanently exposes myosin-binding sites on actin, regardless of calcium concentration. What outcome can most reasonably be predicted?
A researcher engineers a muscle fiber to express a mutant form of tropomyosin that permanently exposes myosin-binding sites on actin, regardless of calcium concentration. What outcome can most reasonably be predicted?
If a researcher introduces a mutation into a skeletal muscle fiber that eliminates the ability of myosin to bind ATP, what would be the most immediate consequence?
If a researcher introduces a mutation into a skeletal muscle fiber that eliminates the ability of myosin to bind ATP, what would be the most immediate consequence?
In a muscle fiber, what would be the immediate effect of a drug that selectively blocks the SERCA pump?
In a muscle fiber, what would be the immediate effect of a drug that selectively blocks the SERCA pump?
Consider a scenario where the T-tubules in a muscle fiber become non-functional due to a genetic defect. How would this primarily affect muscle contraction?
Consider a scenario where the T-tubules in a muscle fiber become non-functional due to a genetic defect. How would this primarily affect muscle contraction?
A scientist discovers a new compound that increases the affinity of troponin for calcium ions. What effect would this compound have on muscle contraction?
A scientist discovers a new compound that increases the affinity of troponin for calcium ions. What effect would this compound have on muscle contraction?
Mutations in the gene encoding dystrophin, a protein that links the cytoskeleton to the extracellular matrix in muscle fibers, are responsible for muscular dystrophy. What immediate effect do these mutations have on muscle contraction?
Mutations in the gene encoding dystrophin, a protein that links the cytoskeleton to the extracellular matrix in muscle fibers, are responsible for muscular dystrophy. What immediate effect do these mutations have on muscle contraction?
A toxin preferentially targets and cleaves the SNARE proteins involved in vesicle fusion at the neuromuscular junction. What immediate effect would this toxin have on skeletal muscle function?
A toxin preferentially targets and cleaves the SNARE proteins involved in vesicle fusion at the neuromuscular junction. What immediate effect would this toxin have on skeletal muscle function?
In a laboratory experiment, a muscle fiber is treated with a drug that selectively permeabilizes the sarcoplasmic reticulum membrane to calcium ions. What downstream effect would this have on muscle contraction?
In a laboratory experiment, a muscle fiber is treated with a drug that selectively permeabilizes the sarcoplasmic reticulum membrane to calcium ions. What downstream effect would this have on muscle contraction?
Suppose a researcher discovers a compound that selectively inhibits the binding of ADP to myosin during the cross-bridge cycle. What would be the immediate consequence of applying this compound to a muscle fiber?
Suppose a researcher discovers a compound that selectively inhibits the binding of ADP to myosin during the cross-bridge cycle. What would be the immediate consequence of applying this compound to a muscle fiber?
A researcher introduces a mutation into a muscle fiber that results in the production of a non-functional ryanodine receptor (RyR). What immediate effect would this have on excitation-contraction coupling?
A researcher introduces a mutation into a muscle fiber that results in the production of a non-functional ryanodine receptor (RyR). What immediate effect would this have on excitation-contraction coupling?
In a hypothetical scenario, a mutation in the gene encoding the voltage-gated sodium channels of a muscle fiber results in channels that open normally but fail to inactivate. What direct effect would this have on the muscle fiber's excitability?
In a hypothetical scenario, a mutation in the gene encoding the voltage-gated sodium channels of a muscle fiber results in channels that open normally but fail to inactivate. What direct effect would this have on the muscle fiber's excitability?
A muscle biopsy reveals a population of fibers with significantly reduced levels of glycogen phosphorylase, the enzyme responsible for glycogen breakdown. How will this most directly affect muscle function during intense exercise?
A muscle biopsy reveals a population of fibers with significantly reduced levels of glycogen phosphorylase, the enzyme responsible for glycogen breakdown. How will this most directly affect muscle function during intense exercise?
Consider a scenario where a novel drug selectively blocks the reuptake of choline at the neuromuscular junction. Which of the following physiological effects is most likely to occur as a direct result of this drug?
Consider a scenario where a novel drug selectively blocks the reuptake of choline at the neuromuscular junction. Which of the following physiological effects is most likely to occur as a direct result of this drug?
A researcher discovers a new toxin that selectively inhibits the release of calcium from the sarcoplasmic reticulum. What immediate effect would this toxin have on skeletal muscle contraction?
A researcher discovers a new toxin that selectively inhibits the release of calcium from the sarcoplasmic reticulum. What immediate effect would this toxin have on skeletal muscle contraction?
A researcher discovers a new molecule that prevents the conformational change in the troponin complex necessary for tropomyosin movement. What immediate effect does this new molecule have on muscle contraction?
A researcher discovers a new molecule that prevents the conformational change in the troponin complex necessary for tropomyosin movement. What immediate effect does this new molecule have on muscle contraction?
Flashcards
Sarcomere
Sarcomere
The region of a myofibril between two consecutive Z discs (or Z-lines); the contractile unit of a muscle fiber.
A-band
A-band
The region composed of thick filaments, where actin and myosin overlap.
H zone
H zone
Contains only thick filaments; the lighter area in the dark A-band.
M line
M line
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I-band
I-band
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Myosin
Myosin
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Myosin heads
Myosin heads
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Actin
Actin
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Tropomyosin
Tropomyosin
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Troponin
Troponin
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Sliding Filament Theory
Sliding Filament Theory
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Neuromuscular Junction (NMJ)
Neuromuscular Junction (NMJ)
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Acetylcholine (ACh)
Acetylcholine (ACh)
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Sarcolemma
Sarcolemma
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Calcium's Role in Contraction
Calcium's Role in Contraction
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T-tubules
T-tubules
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Sarcoplasm
Sarcoplasm
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Excitation-Contraction Coupling
Excitation-Contraction Coupling
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Cross Bridge Formation
Cross Bridge Formation
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Power Stroke
Power Stroke
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Cross Bridge Detachment
Cross Bridge Detachment
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Cocking of Myosin Head
Cocking of Myosin Head
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Muscle Relaxation
Muscle Relaxation
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Rigor Mortis
Rigor Mortis
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Study Notes
Sarcomere Structure
- Myofibrils are contained in muscle fibers, with hundreds existing in each fiber
- Sarcomeres are arranged one after the other within myofibrils
- Sarcomeres contain myofilaments, which can either be thin (actin) or thick (myosin)
- The region of a myofibril between 2 consecutive Z discs (or Z-lines) defines a sarcomere
- Alternating A and I bands provide myofibrils and muscle cells with their striated appearance
- The A-band is the region where thick filaments (myosin) are located, and where actin and myosin overlap
- The H zone contains only thick filaments
- The M line contains proteins that hold the thick filaments together in the middle of the sarcomere
- The I-band has only thin actin filaments
Thick and Thin Filaments
- Thick filaments are made of the protein myosin
- Each myosin molecule has a rod-like tail and two globular heads called the myosin heads
- Myosin heads extend towards the thin filaments and link thick and thin filaments with cross-bridges
- Myosin functions as a motor protein to facilitate the movement of cell structures
- Skeletal muscle contains approximately 300 molecules of myosin in a single thick filament
- In a relaxed muscle, myosin is unable to bind to actin because tropomyosin covers the myosin-binding sites, which are held in place by troponin molecules
Sliding Filament Model
- Thin filaments slide past thick filaments, increasing the overlap between actin and myosin
- In the relaxed state, the thin and thick filaments overlap only slightly
- Myosin heads bind to actin upon stimulation allowing sliding to begin
- Each myosin head binds and detaches several times during contraction, propelling thin filaments to the center of the sarcomere
- Tension is generated as thin filaments are propelled to the center of the sarcomere
- Shortening occurs throughout the sarcomere during this event
- All sarcomeres shorten simultaneously causing the entire muscle fiber to shorten
Neuromuscular Junction
- Skeletal muscles contract when stimulated by a motor neuron
- Muscle cells are stimulated by nerve impulses at the NMJ (Neuromuscular Junction)
- Acetylcholine (Ach) is released from the motor neurons and acts as a neurotransmitter on muscle cells
- Stimulated muscle cells generate and propagate an action potential along their sarcolemma
- This results in a short-lived increase in intracellular calcium levels which triggers muscle contraction
Synapse Steps
- An action potential arrives at the axon terminal of the motor neuron
- Voltage-gated Ca2+ channels open, allowing calcium to move into the neuron
- Synaptic vesicles containing Acetylcholine (Ach) move to the plasma membrane
- Acetylcholine is released into the synaptic cleft, then binds to receptors
- Chemically-gated Na+ channels open, causing an action potential to sweep across the muscle cell membrane and down T-tubules
- The release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm is triggered
Excitation-Contraction Coupling
- The action potential is generated on the sarcolemma and moves down the T-tubules
- Calcium ions are released triggered from the sarcoplasmic reticulum (SR)
- Calcium ions flood the sarcoplasm and bind onto troponin, which causes myosin heads to bind, resulting in muscle contraction
- T-tubules are invaginations of the sarcolemma that bring it into contact with the sarcoplasmic reticulum
- The t-tubules carry the action potential to the interior of the muscle fiber
- Each T-tubule is flanked by sarcoplasmic reticulum
- Action potential in T-tubule triggers calcium channels in the SR to open, resulting in it to diffuse out the SR into the sarcoplasm
Recap of Events
- An action potential arrives at the axon terminal of the pre-synaptic neuron
- Voltage-gated Ca2+ channels open, and calcium moves into the neuron
- Synaptic vesicles containing Acetylcholine move to the plasma membrane
- Acetylcholine is released into the synaptic cleft
- Acetylcholine binds to receptors and causes chemically-gated Na+ channels to open
- The action potential sweeps across the muscle cell membrane and down T-tubules, causing the release of calcium ions from the sarcoplasmic reticulum
Cross-Bridge Cycle steps
- Calcium will bind to troponin which causes tropomyosin to move off of the myosin binding sites on actin
- Myosin bind to actin (forming cross bridges), resulting in a muscle contraction
- ADP and Pi are released causing the myosin heads to pivot moving actin in a power stroke, and active sites become exposed
- Once active sites on actin are now exposed, myosin heads can bind to them and create cross-bridges
- ATP binds to the myosin heads causing them to detach from actin
- Energy gets released from the breakdown of ATP, causing the myosin head to reset, which reactivates the myosin
- Cycle repeats as long as stimulus is present
Stages of the Cross-Bridge Cycle
- Cross Bridge Formation refers to the energized myosin heads binding to actin
- The myosin head is "energized" because it has been primed by ATP from the previous cross-bridge cycle
- Power Stroke refers to ADP and Pi being released causing the myosin head to pivot, which pulls the actin toward the M line
- thin filaments "slide" across the stationary thick filaments during the power stroke
- Cross Bridge Detachment refers to ATP binding which allows the myosin heads to detach from the actin
- Cocking of Myosin Head is the hydrolysis of ATP primes that myosin head, returning it to the "cocked" position and ready to bind actin again
- Steps repeat multiple times during a contraction to pull the thin filaments all the way towards the centre of the sarcomere
Relaxation
- Relaxation occurs once nerve stimulation stops
- Calcium gets actively pumped back into the sarcoplasmic reticulum (using ATP)
- Tropomyosin covers the myosin-binding sites on actin, once again
- Sarcomeres return to the relaxed position
Summary of Events - E-C Coupling
- After stimulation from a motor neuron, an action potential propagates along sarcolemma and down the t-tubules
- Action potential triggers release of calcium from the sarcoplasmic reticulum
- Calcium binds to troponin causing tropomyosin to move away from the myosin binding sites on actin
- Contraction follows
Summary of Events - Contraction
- Cross-bridge formation has energized myosin heads attaching to the actin filament
- Power stroke has myosin heads pivoting which pulls thin filaments toward center of sarcomere
- Cross-bridge detachment has ATP binding and detaching myosin from actin
- Cocking of myosin head is the hydrolysis of ATP which provides the energy to prime myosin head for next cycle
Summary of Events - Relaxation
- Calcium gets pumped back into the sarcoplasmic reticulum done via active transport that requires ATP
- All cross-bridges get released as tropomyosin moves back into its blocking position
- Actin and myosin are ready to interact again once stimulated by a neuron
Roles of ATP
- ATP is needed to detach myosin heads from actin in the cross-bridge cycle and prime them for the next
- ATP is used to pump calcium back out of the sarcoplasm
- Without ATP, myosin would be unable to release from actin, resulting in muscle contraction
Rigor Mortis
- Dying cells lose their ability to keep calcium out of the cell
- Calcium rushes in from the extracellular fluid which promotes binding of myosin to actin
- No more ATP is being produced
- Myosin and actin cannot detach, and calcium ions cannot be pumped out of the cell, leading to muscle rigidity
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