Neuromuscular Junction: Structure and Mechanism - Anatomy and Physiology
- What happens to the choline released when ACh is broken down?
- It is taken back into the axon terminal and reused to synthesize new ACh.
- A drug inhibits acetylcholinesterase. What happens to ACh at the neuromuscular junction?
- ACh stays in the cleft longer and keeps stimulating receptors, which is why these drugs can treat myasthenia gravis.
- What type of receptor does ACh bind on the motor end plate?
- Nicotinic ACh receptors, which are ligand-gated cation channels.
- How does curare cause paralysis?
- It competitively blocks nicotinic ACh receptors on the motor end plate, so ACh cannot depolarize the muscle fiber.
- What is the function of the junctional folds of the motor end plate?
- They increase the surface area of the sarcolemma, providing room for many ACh receptors.
- Which enzyme ends the action of ACh at the neuromuscular junction?
- Acetylcholinesterase in the synaptic cleft, which breaks ACh into acetate and choline.
- What opens in the axon terminal when an action potential arrives, triggering ACh release?
- Voltage-gated calcium channels. Calcium entry causes synaptic vesicles to release ACh by exocytosis.
- Which bacterial toxin causes flaccid paralysis by preventing ACh release from motor axon terminals?
- Botulinum toxin. It blocks the fusion of ACh vesicles with the terminal membrane.
- Autoantibodies destroy ACh receptors on the motor end plate, causing weakness that worsens with use. What is the disorder?
- Myasthenia gravis. Fewer receptors mean smaller end plate potentials that may fail to reach threshold.
- How many neuromuscular junctions does a typical skeletal muscle fiber have?
- One, usually located near the middle of the fiber.
- Which neurotransmitter is released at the skeletal neuromuscular junction?
- Acetylcholine (ACh).
- What is the end plate potential?
- A local depolarization of the motor end plate caused mainly by Na+ entering through ACh receptor channels; it normally reaches threshold.