Electrical Excitability - Synaptic Transmission and the Neuromuscular Junction Flashcards
How is a signal passed from nerve to muscle?
An action potential travels via the nerve and arrives at the neuromuscular junction.
What is the neuromuscular junction?
The synapse between a nerve and a skeletal muscle fibre.
Why is the action potential important by the synapse?
It activates voltage-gated Ca2+ channels which in their turn will activate vesicular transport to cause a neurotransmitter encapsulated in the vesicle to be released into the synaptic cleft.
What is a consequence of an increased frequency of action potentials?
It will increase the amount of Ca2+ that enters the synapse which means more neurotransmitters will be released.
What is the structure of a voltage-gated Ca2+ channel?
Very similar structure to voltage-gated Na+ channels. ! subunit consisting of 4 sections. A pore. A voltage sensing region.
How do voltage-gated Ca2+ channels and voltage-gated Na+ channels differ?
VGCCs activate more slowly than VGNaCs.
VGCCs activate and inactivate but much slower than VGNaCs. VGCCs’ inactivation is dependent on Ca2+ themselves.
What is acetylcholine esterase?
An enzyme breaking down ACh. Important in order to not have ACh at all times in the synaptic cleft.
Briefly explain transmitter release.
Ca2+ enter through VGCCs.
Ca2+ binds to synaptotagmin.
Vesicles are therefore brought close to membrane
Snare complex make a fusion pore
Transmitters are released via the fusion pore.
What kind of channel is a nicotinic acetylcholine receptor?
A ligand-gated ion channel
What is the nicotinic acetylcholine receptor channel (the ligand-gated ion channel) permeable to?
Cations like K+ and Na+.
What is the purpose of the acetylcholine receptors on the muscle fibre?
As they are opened there is an influx of Na+ which causes a brief depolarisation of the muscle fibres’ plasma membrane causing a muscle action potential to spread.
What kind of blockers are there that will prevent an action potential in the muscle fibres? How do they work?
Competitive blockers blocks the site where acetylcholine is supposed to bind on the nicotinic acetylcholine receptor. Na+ can’t enter.
Depolarising blockers inactivates Na+ channels. These Na+ channels are not the same channels that acetylcholine binds to. They are the channels that are activated by the brief spark in Na+ concentration from the nAChR
Give an example of a competitive blocker.
D-tubocurarine
Give an example of a depolarising blocker.
Succinylcholine
Why would you use neuromuscular blocking agents?
To help with surgery. It doesn’t relieve pain as general anaesthesia do though! They are used to cause temporary paralysis.
