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Questions and Answers
What is the primary physiological mechanism that links electrical discharge in muscle to muscle contraction?
What is the primary physiological mechanism that links electrical discharge in muscle to muscle contraction?
What occurs at the motor end plate of the skeletal muscle fiber?
What occurs at the motor end plate of the skeletal muscle fiber?
What is the effect of depolarization below threshold at the neuromuscular junction?
What is the effect of depolarization below threshold at the neuromuscular junction?
Which ion's release is crucial for muscle contraction following electrical activation?
Which ion's release is crucial for muscle contraction following electrical activation?
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What role do motor axons play at the neuromuscular junction?
What role do motor axons play at the neuromuscular junction?
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What role does the Ca-ATPase pump play in muscle contraction?
What role does the Ca-ATPase pump play in muscle contraction?
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During the excitation-contraction coupling, which event occurs first?
During the excitation-contraction coupling, which event occurs first?
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What percentage of ATP is used by the Ca-ATPase pump during muscle relaxation?
What percentage of ATP is used by the Ca-ATPase pump during muscle relaxation?
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What happens when action potentials cease in muscle fibers?
What happens when action potentials cease in muscle fibers?
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In the process of cross-bridge cycling, what is the sequence of events?
In the process of cross-bridge cycling, what is the sequence of events?
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What is the primary function of Acetycholinesterase inhibitors in treating Myasthenia gravis?
What is the primary function of Acetycholinesterase inhibitors in treating Myasthenia gravis?
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How does botulism toxin affect muscle contraction?
How does botulism toxin affect muscle contraction?
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What occurs to calcium ions during muscle contraction?
What occurs to calcium ions during muscle contraction?
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Which treatment method is NOT associated with the management of Myasthenia gravis?
Which treatment method is NOT associated with the management of Myasthenia gravis?
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What is the role of the sarcoplasmic reticulum in muscle fibers?
What is the role of the sarcoplasmic reticulum in muscle fibers?
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What is a common symptom associated with Myasthenia gravis?
What is a common symptom associated with Myasthenia gravis?
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What best describes the Transverse Tubules (T-tubules) in muscle fibers?
What best describes the Transverse Tubules (T-tubules) in muscle fibers?
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How does curare affect muscle function?
How does curare affect muscle function?
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Study Notes
Skeletal Muscle: Structure & Function II
- Lecture: MD137: Principles of Physiology, Dr. K.McCullagh, 2024
- Topic: Electrical activation of muscle contraction, excitation-contraction coupling, neuromuscular junction, and clinical relevance.
Neuromuscular Junction (NMJ)
- Location: The site where a motor neuron stimulates a muscle fiber.
- Structure: Image shows somatic motor neuron axon and skeletal muscle fibers connected by many neuromuscular junctions (NMJs).
Excitation-Contraction Coupling
- Mechanism: A physiological process where an electrical discharge at the muscle initiates chemical events at the cell surface. This releases intracellular Ca²⁺, producing muscle action.
Excitation-Contraction Coupling Steps
- Step 1: Acetylcholine (ACh) is released from the somatic motor neuron.
- Step 2: ACh binds to nicotinic ACh receptors, causing ligand-gated channels to open.
- Step 3: Sodium (Na⁺) diffuses inwards, creating a depolarizing stimulus.
- Step 4: An action potential is produced.
- Step 5: The action potential travels along transverse tubules (T-tubules).
- Step 6: Voltage-gated calcium (Ca²⁺) channels open.
- Step 7: Ca²⁺ is released from the sarcoplasmic reticulum (SR).
- 8: Ca²⁺ binds to troponin, causing a shift in tropomyosin, exposing myosin-binding sites on actin filaments.
- Step 9: Cross-bridges form between actin and myosin.
- Step 10: Myosin heads rotate and generate force.
- Step 11: Muscle contraction ensues.
Neuromuscular Junctions & Motor End Plates
- Motor end plate: The area of the muscle fiber sarcolemma where a motor neuron stimulates it.
- Components: Parts like motor neuron axon, muscle fiber nucleus, nerve fiber branches, synaptic vesicles and synaptic cleft are features of this structure.
The Neuromuscular Junction (Detailed)
- Step 1: Motor neuron action potential arrives.
- Step 2: Calcium (Ca²⁺) enters the axon terminal.
- Step 3: Acetylcholine (ACh) vesicles fuse with the membrane and release ACh into the synaptic cleft.
- Step 4: ACh binds to receptors on the motor end plate, opening ion channels.
- Step 5: Sodium (Na⁺) enters the muscle fiber, generating an end-plate potential (EPP).
- Step 6: The EPP initiates an action potential in the muscle fiber.
- Step 7: Muscle fiber action potential travels along the sarcolemma and into T-tubules.
- Step 8: Depolarization of the T-tubules triggers release of Ca²⁺ from the sarcoplasmic reticulum.
- Step 9: Ca²⁺ initiates the contraction.
Structural Features of the Neuromuscular Junction
- Components: Schwann cell, synaptic vesicles, synaptic cleft, postjunctional fold, and nicotinic acetylcholine receptors (on the postjunctional membrane) are parts of NMJ.
Electrical Activity at the Neuromuscular Junction
- Chemical transmitter release: Neurotransmitter (ACh) is released at nerve terminal, triggering signal.
- Inward membrane current: This current flows into motor end plate.
- End plate potential (EPP): Produced by inward current, it's a depolarization.
Electrical Activity at the Neuromuscular Junction (cont.)
- Many motor axon action potentials: This produces an EPP that can trigger muscle contraction.
- Na⁺ channel threshold: Action potential occurs when the EPP depolarization surpasses the Na+ channel threshold.
Clinical Implications
- Substance affecting ACh transmission: Impacts muscle contraction.
- Botulinum toxin (Botox): Used for various conditions (dystonias, cerebral palsy). It inhibits ACh release.
- Curare: A poison arrow toxin blocking ACh receptors.
- Acetylcholinesterase inhibitors: Used for myasthenia gravis (e.g., neostigmine) to increase available ACh.
Myasthenia Gravis
- Autoimmune disease: The immune system attacks ACh receptors at the neuromuscular junction.
- Symptoms: Muscle weakness (e.g., eye and limb muscles).
- Incidence: Approximately 1 in 5000 people.
- Treatment: Acetylcholinesterase inhibitors, plasmapheresis.
Acetylcholinesterase Inhibitors
- Mechanism: Prevents breakdown of ACh in the synaptic cleft. Increases ACh levels which compensates for the low numbers of ACh receptors in myasthenia gravis.
- Example: Neostigmine
Stimulating a Muscle Contraction
- Acetylcholine release: From the motor neuron.
- End plate potentials: Produced at the motor end plate.
- Action potentials: Generated in the muscle.
- Calcium release: Voltage gated calcium channels (DHPRs)in Transverse tubules change shape triggering sarcoplasmic reticulum channels to open.
- Cross-bridge cycling: Binding, rotating and generating force, using ATP.
Muscle Relaxation
- Action potentials cease: Electrical signals stop.
- Calcium reuptake: Ca²+ is pumped back into SR by Ca²+ -ATPase pump..
- Cross-bridge release: No more Ca²⁺ is available to bind to troponin C, so cross-bridges detach.
Excitation-Contraction Coupling (Summary)
- Sequence of events: Depolarization, calcium release, cross-bridge formation, rotation, and force creation.
- Temporal relationship: Action potential precedes Ca²⁺ increase, which precedes contractile force generation.
Sarcoplasmic Reticulum (SR)
- Function: Stores Ca²⁺ when muscle is at rest
- Calcium release: SR releases Ca²⁺ when muscle is stimulated.
- Mechanism: This release is via RyR (ryanodine receptors).
- Calcium reuptake: Ca²⁺ is actively pumped back into SR by sarcoplasmic reticulum (SR) Ca²⁺-ATPase pumps.
Transverse Tubules (T-tubules)
- Structure: Membrane tunnels from sarcolemma. Have access to extracellular environment.
- Function: Conduct action potentials deep within the muscle fiber.
Myofibrils and Sarcoplasmic Reticulum (SR)
- Structures: Components involved in muscular contraction.
- Relationship: Myofibrils are composed of filaments and related to the sarcoplasmic reticulum (SR) which is modified endoplasmic reticulum.
Dihydropyridine Receptor (DHP)
- Integral membrane protein: Present in the transverse tubules (T-tubules) of muscle cells.
- Coupling mechanism: DHP receptor contributes to the excitation-contraction coupling, which is the process that links muscle excitation to contraction.
- Related components: DHP receptors interact with ryanodine receptors.
Ca²⁺-ATPase Pump
- Function: Pumps Ca²⁺ back into the sarcoplasmic reticulum (SR) after contraction.
- ATP requirement: This process uses a significant amount of ATP to maintain calcium levels.
- Regulation: Actively regulates calcium levels, ensuring muscle relaxation.
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Description
Explore the intricate details of skeletal muscle structure and function in this quiz. Covering the neuromuscular junction and the process of excitation-contraction coupling, this quiz will challenge your understanding of muscle physiology. Relevant for MD137 Principles of Physiology, it tests your knowledge on muscle activation and its clinical relevance.