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Questions and Answers
What initiates the release of intracellular Ca2+ during excitation-contraction coupling?
What initiates the release of intracellular Ca2+ during excitation-contraction coupling?
What is the role of the motor end plate in muscle contraction?
What is the role of the motor end plate in muscle contraction?
What occurs during the excitatory postsynaptic potential (EPSP) at the neuromuscular junction?
What occurs during the excitatory postsynaptic potential (EPSP) at the neuromuscular junction?
What is the primary consequence of the electrical discharge at the neuromuscular junction?
What is the primary consequence of the electrical discharge at the neuromuscular junction?
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Which of the following best describes the function of the neuromuscular junction?
Which of the following best describes the function of the neuromuscular junction?
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What triggers the opening of calcium channels in the sarcoplasmic reticulum during muscle contraction?
What triggers the opening of calcium channels in the sarcoplasmic reticulum during muscle contraction?
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How does muscle relaxation occur after a contraction?
How does muscle relaxation occur after a contraction?
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What role do cross-bridges play in muscle contraction?
What role do cross-bridges play in muscle contraction?
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What percentage of ATP is used for the Ca2+-ATPase pump during muscle relaxation?
What percentage of ATP is used for the Ca2+-ATPase pump during muscle relaxation?
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Which sequence of events correctly describes excitation-contraction coupling?
Which sequence of events correctly describes excitation-contraction coupling?
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What is the primary effect of Acetycholinesterase inhibitors in treating Myasthenia gravis?
What is the primary effect of Acetycholinesterase inhibitors in treating Myasthenia gravis?
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What substance is used in cosmetic surgery to inhibit acetylcholine release?
What substance is used in cosmetic surgery to inhibit acetylcholine release?
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How does curare affect muscle contractions?
How does curare affect muscle contractions?
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What happens to calcium ions during muscle relaxation?
What happens to calcium ions during muscle relaxation?
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In Myasthenia gravis, which mechanism leads to the symptoms of grave muscle weakness?
In Myasthenia gravis, which mechanism leads to the symptoms of grave muscle weakness?
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Which process involves the opening of calcium release channels in muscle fibers?
Which process involves the opening of calcium release channels in muscle fibers?
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What is the primary role of the transverse tubules in muscle fibers?
What is the primary role of the transverse tubules in muscle fibers?
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What characterizes the sarcoplasmic reticulum in muscle cells?
What characterizes the sarcoplasmic reticulum in muscle cells?
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Study Notes
Skeletal Muscle: Structure & Function II
- MD137: Principles of Physiology lecture covers the steps of electrical activation of muscle contraction, excitation-contraction coupling, and the neuromuscular junction. Clinical relevance is also discussed.
The Neuromuscular Junction (NMJ)
- The NMJ is where a motor neuron stimulates a muscle fiber.
- This area shows somatic motor neuron axon and skeletal muscle fibers with neuromuscular junctions (NMJs)
Excitation-Contraction Coupling
- A physiological mechanism where an electrical discharge at the muscle initiates chemical events that release intracellular Ca²⁺ and cause muscle action.
Steps of Excitation-Contraction Coupling
- Neurotransmitter Release: Acetylcholine (ACh) is released from the somatic motor neuron.
- ACh Binding: ACh binds to nicotinic ACh receptors, opening ligand-gated channels.
- Sodium Influx: Sodium (Na⁺) diffuses into the muscle fiber, creating a depolarizing stimulus.
- Action Potential Generation: An action potential is produced.
- Action Potential Propagation: Action potentials are conducted along the transverse tubules (T-tubules).
- Calcium Release: Action potentials open voltage-gated calcium (Ca²⁺) channels. Ca²⁺ is released from the sarcoplasmic reticulum (SR).
- Calcium Binding: Ca²⁺ binds to troponin, allowing actin-myosin cross-bridges to form.
- Muscle Contraction: Cross-bridges bind, rotate, and generate force.
- Calcium Removal: Ca²⁺ is actively pumped back into the sarcoplasmic reticulum (SR) by the Ca²⁺-ATPase pump.
- Muscle Relaxation: No more Ca²⁺ is available, so the muscle fiber relaxes.
Neuromuscular Junctions and Motor End Plates
- Neuromuscular junction: The site where a motor neuron stimulates a muscle fiber.
- Motor end plate: The area of the muscle fiber's sarcolemma where a motor neuron stimulates it.
The Neuromuscular Junction (Detailed)
- Motor neuron action potential: Initiates the process.
- Calcium entry: Calcium enters voltage-gated channels.
- Acetylcholine release: Acetylcholine is released into the synaptic cleft.
- Acetylcholine binding: Acetylcholine binds to receptors on the muscle fiber.
- Sodium entry: Sodium enters, generating an action potential.
- Muscle action potential: Propagated along the muscle fiber's membrane.
- Calcium release: Calcium is released from the sarcoplasmic reticulum.
- Muscle contraction: Calcium binding triggers muscle contraction.
- Acetylcholine degradation: Acetylcholinesterase breaks down acetylcholine.
Structural Features of the Neuromuscular Junction
- Schwann cell: Encloses and isolates the axon terminal.
- Synaptic vesicles: Contain acetylcholine (ACh).
- Synaptic cleft: The gap between the neuron and muscle fiber.
- Postjunctional fold: Increases the surface area of the muscle fiber membrane.
- Nicotinic acetylcholine receptors: Molecules that bind to ACh.
Electrical Activity at the Neuromuscular Junction
- Chemical transmitter release: Motor axon action potential triggers release of acetylcholine into the synaptic cleft
- Inward membrane current: Acetylcholine binding leads to sodium ion inward current, generating an excitatory postsynaptic potential (EPSP).
- Depolarization below threshold: EPSP not strong enough to trigger a full action potential.
Electrical Activity at the Neuromuscular Junction (Continued)
- Many motor axon action potentials: Repeated signals create numerous EPSPs, each summating to reach the action potential threshold.
- Na⁺ channel threshold: Action potential is triggered when sodium channels open above a critical threshold.
Clinical Implications
- Substances affecting acetylcholine transmission affect muscle contraction.
- Botulism toxin (Botox) inhibits acetylcholine release, used for various medical conditions.
- Curare blocks acetylcholine receptors, found in poison arrows.
- Acetylcholinesterase inhibitors treat myasthenia gravis (muscle weakness due to insufficient acetylcholine).
Myasthenia Gravis (Grave Muscle Weakness)
- An autoimmune disease where the immune system attacks acetylcholine receptors at the neuromuscular junction.
- Incidence: 1 in 5000 people.
- Treatment: Acetylcholinesterase inhibitors (e.g., neostigmine) and plasmapheresis (plasma exchange).
Acetylcholinesterase Inhibitors
- Inhibition mechanism: Prevents breakdown of acetylcholine (ACh).
- Result: High ACh concentration in synaptic cleft, compensating for reduced receptor numbers.
Excitation-Contraction Coupling (Summary)
- Begins with an action potential.
- Leads to calcium release.
- Cross-bridging and muscle contraction are activated.
- Relaxation occurs through calcium reabsorption.
Transverse Tubules
- Narrow membranous tunnels from sarcolemma.
- Open to extracellular environment.
- Conducts action potentials.
Sarcoplasmic Reticulum (SR)
- Stores Ca²⁺ when muscle is at rest.
- Releases Ca²⁺ through RyR (ryanodine receptor) channels when stimulated.
- Actively pumps Ca²⁺ back into the SR during relaxation.
Myofibrils and Sarcoplasmic Reticulum
- Myofibrils contain actin and myosin filaments, involved in muscle contraction.
- SR surrounds the myofibrils.
- Structures are visualized in the provided image.
Temporal Sequence of Events
- Action potential precedes the increase in intracellular calcium (Ca²⁺).
- Calcium increase precedes cross-bridge cycling and force generation.
Stimulating a Muscle Contraction
- Acetylcholine is released .
- End-plate potentials (EPPs) are created.
- Action potentials are generated.
- Ca2+ channels in transverse tubules (T-tubules) are opened by the altered shape of DHPRs on the T-tubules
- Ca2+ release from sarcoplasmic reticulum (SR)
Muscle Relaxation
- Action potentials stop.
- Ca²⁺-ATPase pumps Ca²⁺ back into the SR.
- No more calcium is available for cross-bridge attachment
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Description
Test your knowledge on the structure and function of skeletal muscle, focusing on electrical activation and excitation-contraction coupling. This quiz covers the neuromuscular junction and its clinical relevance, highlighting key processes involved in muscle contraction.