ICCP S7 Synaptic Transmission And The Neuromuscular Junction Flashcards
In terms of neurone structure where do action potentials originate?
EPSPs build up to generate an action potential at the axon hillock
What does increased frequency of action potentials lead to?
More Ca2+ entering nerve terminal and therefore more NT release.
Describe the structure of the alpha-subunit of voltage gates Ca2+ channels
Give an example of a calcium ion channel blocker.
4 repeats
6TM domains per repeat
4th TM domain is voltage sensor
Intracellular N and C terminus
Nifedipine
What is the subunit composition of Na+ and Ca2+ channels?
Alpha, beta 1 and beta 2 sub units in Na+ channel
alpha, alpha 2, beta gamma and delta subunits in Ca2+ channel.
What is necessary for a functioning channel?
What are the roles of other associated sub units?
A pore forming subunit
- The alpha subunit.
Fine tune and correct regulation of channel activity.
What can be said about activation and inactivation speed of Ca2+ channels compared to Na+?
What is meant by ‘Ca2+ channels inaction is Ca2+ dependant”?
Slower
Altogether another group 2 metal ie barium can flow through them, when it does, less inactivation is seen?
Describe how Ca2+ causes NT release.
Ca2+ binds to synaptotagmin
Causes vesicles to be bought to membrane and bind to synaptotagmin
Snare complex forms which forms a fusion pore.
NT released through pore.
How many ACh bind to nAChR?
What is the relationship between end-plate potentials amplitude and extrernal Ca2+ concentration?
2
As external [Ca2+] decreases so does amplitude of end-plate potential.
Name a competitive nAChR blocker.
What can it cause?
Tubocurarine
Paralysis
Name a depolarising nAChR blocker.
Describe how depolarising blockers work.
Succinylcholine
Bind with higher affinity than ACh to nAChRs and maintain depolarisation by keeping the voltage gated Na+ channels opened leading to the inactivation of these channels.
What is myasthenia gravis and what is it caused by?
Autoimmune disease that targets nAChRs resulting in muscle weakness and fatigue.
Caused by antibodies that bind to nAChR on postsynaptic membrane of skeletal muscle .
Loss of nAChRs by complement mediated lysis and receptor degradation.
Endplate potentials are reduced in amplitude leading to muscle weakness and fatigue.
How is myasthenia gravis treated?
Treated by using ACh esterase blockers which will increase cause ACh concentration in the synaptic cleft.
Allows for increased time for interaction with nAChRs allowing for endplate potential to reach threshold.
Why do mAChRs produce a slower response compared to nAChRs?
because they are GPCRs and therefore trigger a cascade of events in the cell.
