Describe the effect of the botulinum toxin, which inhibits the release of acetylcholine at the neuromuscular junction. Would the poison curare, which competes for acetylcholine receptors (by attaching to the acetylcholine receptors and preventing acetylcholine from binding) have a similar effect? Explain

Describe the effect of the botulinum toxin, which inhibits the release of acetylcholine at the neuromuscular junction. Would the poison curare, which competes for acetylcholine receptors (by attaching to the acetylcholine receptors and preventing acetylcholine from binding) have a similar effect? Explain

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter7: The Peripheral Nervous System: Efferent Division

Section: Chapter Questions

Problem 4RE

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In the rare neuromuscular disorder Myasthenia Gravis, autoantibodies are produced which inhibit acetylcholine receptor (nicotinic receptor) activity. Explain how inhibition of acetylcholine receptor activity at the neuromuscular junction will affect the sequence of events in muscular excitation and contraction in response to stimuli, and muscle function? (Mention the effects on all the significant events involved in excitation and contraction of muscles, and how it would affect muscle function).
What could happen if you block the binding of acetylcholine to its receptors at the neuromuscular junction?
When curare, a neuromuscular poison, is dropped onto an isolated muscle-nerve preparation in a laboratory, the muscle does not contract when the nerve is stimulated, even though neurotransmitter is released from the nerve cell. Why does this happen? How might this action of curare be lethal to an individual who has been poisoned?
If a patient was bitten by a poisonous spider (black widow) and the effects of its venom occurred at the neuromuscular junction in the peripheral nervous system, what neurotransmitter would be affected by this venom? And explain the mechanism of action of how the venom is a direct antagonist to this neurotransmitter.
When the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation. How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?
Caffeine prolongs the life span of acetylcholine molecules in the motor junctions. Explain how this fact is related to caffeine’s tendency to cause jitters, such as hand tremors and other small involuntary contractions.
Give an account of signalling at a neuromuscular junction through the nicotinic acetylcholine receptor.
hen an action potential arrives at the nerve terminal of a neuromuscular junction, which of the following statements best describes the events that occur? Depolarisation of the nerve terminal causes the release of ACh which activates nicotinic receptors on the skeletal muscle membrane to cause Ca2+ entry and muscle contraction. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which activates voltage-gated Na+ channels at the end-plate. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which binds to muscarinic receptors at the end plate. Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores…
A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.
Why is it important to remove acetylcholine from its binding to acetylcholine receptors once the neural stimulus ends? What can be the possible consequence of the non-removal of acetylcholine to the skeletal muscle fiber?
ATPase is an enzyme that can hydrolyse ATP and release the potential energy stored in the phosphate bond. How would a metabolic inhibitor that blocks ATPase function affect the resting potential of nerve cells?
Motor neurons release what type of neurotransmitter onto the motor end plate of skeletal muscles? What effect does this neurotransmitter have on the postsynaptic membrane?