Podcast
Questions and Answers
What is the primary role of acetylcholinesterase (AChE) in muscle relaxation?
What is the primary role of acetylcholinesterase (AChE) in muscle relaxation?
- To facilitate the binding of ATP to myosin heads.
- To actively transport calcium ions back into the sarcoplasmic reticulum.
- To bind with acetylcholine receptors on the motor end plate.
- To break down acetylcholine into acetic acid and choline, terminating its effect. (correct)
Which of the following is the most direct role of ATP in muscle relaxation?
Which of the following is the most direct role of ATP in muscle relaxation?
- Causing the detachment of myosin heads from actin. (correct)
- Hydrolyzing acetylcholine.
- Regeneration of acetylcholine at the neuromuscular junction.
- Pumping calcium ions into the sarcoplasmic reticulum.
How does the sarcoplasmic reticulum contribute to muscle relaxation?
How does the sarcoplasmic reticulum contribute to muscle relaxation?
- By releasing acetylcholine to stimulate muscle fibers.
- By actively transporting calcium ions out of the sarcoplasm. (correct)
- By releasing sodium ions to repolarize the muscle cell membrane.
- By breaking down ATP to reduce the energy supply to the muscle.
What event immediately leads to tropomyosin covering the myosin binding sites on actin during muscle relaxation?
What event immediately leads to tropomyosin covering the myosin binding sites on actin during muscle relaxation?
During muscle relaxation, what happens to the choline that results from the breakdown of acetylcholine?
During muscle relaxation, what happens to the choline that results from the breakdown of acetylcholine?
Apart from muscle contraction and relaxation, what other process requires the use of ATP within muscle fibers?
Apart from muscle contraction and relaxation, what other process requires the use of ATP within muscle fibers?
Rigor mortis is primarily caused by:
Rigor mortis is primarily caused by:
Why do muscle membranes become 'leaky' after death, contributing to rigor mortis?
Why do muscle membranes become 'leaky' after death, contributing to rigor mortis?
How does the presence of calcium ions contribute to rigor mortis?
How does the presence of calcium ions contribute to rigor mortis?
Approximately how long after death does rigor mortis typically begin?
Approximately how long after death does rigor mortis typically begin?
What is the underlying cause of muscle weakness in Myasthenia Gravis?
What is the underlying cause of muscle weakness in Myasthenia Gravis?
How do acetylcholinesterase inhibitors alleviate symptoms of Myasthenia Gravis?
How do acetylcholinesterase inhibitors alleviate symptoms of Myasthenia Gravis?
What is the mechanism by which botulinum toxin causes flaccid paralysis?
What is the mechanism by which botulinum toxin causes flaccid paralysis?
Why does low extracellular calcium lead to muscle cramps?
Why does low extracellular calcium lead to muscle cramps?
How does nicotine affect skeletal muscles?
How does nicotine affect skeletal muscles?
What is the primary effect of black widow spider venom on acetylcholine release?
What is the primary effect of black widow spider venom on acetylcholine release?
What is the long-term effect of black widow spider venom on acetylcholine receptors?
What is the long-term effect of black widow spider venom on acetylcholine receptors?
What is the primary mechanism of curare poisoning?
What is the primary mechanism of curare poisoning?
Which of the following best describes how curare affects muscle function?
Which of the following best describes how curare affects muscle function?
Why is curare sometimes used during surgical procedures?
Why is curare sometimes used during surgical procedures?
Flashcards
Acetylcholinesterase (AChE)
Acetylcholinesterase (AChE)
Breaks down acetylcholine at the motor end plate into acetic acid and choline to terminate the signal.
Ca2+ - ATPase Pumps
Ca2+ - ATPase Pumps
These actively pump calcium back into the sarcoplasmic reticulum to lower sarcoplasmic calcium levels.
ATP Role in Relaxation
ATP Role in Relaxation
ATP binding to the myosin head causes it to detach from the actin binding site to allow for muscle relaxation.
Tropomyosin's Role in Relaxation
Tropomyosin's Role in Relaxation
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ATP Needs in Muscle Function
ATP Needs in Muscle Function
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Rigor Mortis
Rigor Mortis
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Myasthenia Gravis
Myasthenia Gravis
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Botulinum Toxin (Botox)
Botulinum Toxin (Botox)
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Low Extracellular Calcium Effects
Low Extracellular Calcium Effects
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Nicotine's Muscle Effects
Nicotine's Muscle Effects
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Black Widow Spider Venom
Black Widow Spider Venom
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Curare Poisoning
Curare Poisoning
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Study Notes
Relaxation
- Acetylcholine is broken down by acetylcholinesterase (AChE)
- AChE is located on the motor end plate
- The breakdown of acetylcholine results in acetic acid and choline
- Acetic acid enters the Kreb's cycle, releasing energy through catabolism
- Choline is recycled to build other molecules
- The sarcoplasmic reticulum actively uptakes calcium ions (Ca2+)
- Ca2+ ATPase pumps calcium from the sarcoplasm into the sarcoplasmic reticulum
- ATP binding causes myosin heads to detach from myosin binding sites on actin
- Tropomyosin returns to its resting position, covering myosin binding sites on actin
ATP Functions in Muscles
- ATP is required for:
- Activation of myosin and the power stroke
- Release of the cross-bridge, allowing muscle relaxation
- Ca2+ ATPase activity, which pumps calcium back into the sarcoplasmic reticulum
- Maintaining the Na+/K+ ATPase, which helps restore Na+ and K+ gradients after an action potential
Rigor Mortis
- Myosin heads are active in relaxed muscle, ready to bind actin when myosin binding sites are exposed
- After death, ATP production ceases, halting breathing and oxygen delivery for the electron transport chain
- Membranes become leaky after death, resulting in the sarcoplasmic reticulum and extracellular fluid releasing calcium into the sarcoplasm
- Ca2+ binds to troponin, causing tropomyosin to expose myosin binding sites on actin
- Cross-bridges form, but without ATP, myosin heads cannot detach from actin, leading to a contracted state
- Rigor mortis begins approximately 3 hours post-mortem and peaks at 12 hours
- Rigor mortis gradually subsides as cells decompose over a few days
Clinical Applications of the Neuromuscular Junction
- Myasthenia gravis is caused by a decrease in acetylcholine receptors and is an autoimmune disease
- It is treated with acetylcholinesterase inhibitors to increase acetylcholine binding to the remaining receptors
- Botulism can result from improper canning and is caused by infection with Clostridium botulinum
- Clostridium botulinum produces botulinum toxin ("botox")
- Botulinum toxin inhibits acetylcholine exocytosis, resulting in flaccid paralysis
- Botox is clinically used for crossed eyes and uncontrollable blinking
- Botox has cosmetic applications to control wrinkles and sweating
- Low extracellular calcium leads to decreased stabilization of Na+ gated channels
- The opening of Na+ gated channels leads to muscle cell depolarization, causing cramps
- Nicotine binds to acetylcholine receptors
- Nicotine mimics acetylcholine effects and causes muscle spasms
- Black widow spider venom causes a massive release of acetylcholine, and muscle contraction and stops breathing
- It initially stimulates acetylcholine receptors, but in the long term, it can lead to receptor desensitization and depressed muscle firing
- Curare poisoning prevents acetylcholine binding to its receptors
- Curare poisoning causes flaccid paralysis and it is used in surgeries
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