M&R 5.1 - Cellular Response to Action Potentials Flashcards Preview

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Flashcards in M&R 5.1 - Cellular Response to Action Potentials Deck (17):

How do action potentials open vg Ca2+ channels?

- Depolarisation = opening

- Ca2+ influx inwards due to large concentration gradient


Describe the structure of vg Ca2+ channels

- Very similar to Na+ channels (specifically the alpha subunit, the pore forming subunit)

- 4 repeats with a voltage sensor

- Some repeats have phosphorylation sites which alter its activity e.g. cardiac muscle


Describe the diversity of vg Ca2+ channels

- Very diverse

- Found in skeletal muscle, neurones, lungs etc.

- L types are clinically relevant


Why are L-type vg channels clinically relevant?

They can be targeted due to their different structures and are susceptible to blockers


What is the function of the mitochondria at the motor end plate?

Remove residual Ca2+ that is left over from the action potential


What is the function of Acetylcholinesterase at the motor end plate?

Quickly breaks down Acetylcholine


What is the function of vesicles at the motor end plate?

- Contain a high concentration of Acetylcholine

- Ca2+ influx due to action potenital = release of Ach by exocytosis


Describe the process of transmitter release from a vesicle

• Ca2+ entry through Ca2+ channels

• Ca2+ binds to synaptotagmin (Ca2+ channels close)

• Vesicle brought close to membrane due to binding

• Snare complex make a fusion pore causing vesicle to be continuous with the extra cellular space

• Transmitter released through this pore


What happens after Ach has been released into the synaptic cleft?

- Ach diffuses across and binds to the nicotinic Ach receptors on the post-junctional membrane

- Produces an end-plate potential

- Excess is broken down by Acetylcholinesterase


What happens after the binding of the Ach to the nicotinic receptors?

- End plate potential is produced due to depolarisation (K+ exit is overcome)

- Raises membrane potential closer to Ena


Describe the structure of a nicotinic Ach receptor

- 2 alpha subunits

- 5 subunits

- Binds 2 molecules of Ach to cause a conformational change


Describe the action of competitive antagonists such as Tubocurarine on nicotinic Ach receptors

- Similar structure to Ach so sits in binding site

- Doesn't produce a conformational change so remains closed (doesn't activate)

- Reversible so can be overcome by a high Ach concentration


Describe the action of depolarising blockers such as Succinylcholine on nicotinic Ach receptors

- Binds and activates nicotinic receptors

- Maintains depolarisation

- Causes accommodation to happen so Na+ channels are inactive


What is Myasthenia Gravis? How does it present?

- An autoimmune disease targeting nAch receptors

- Profound weakness that increases with exercise


What mechanism of action for myasthenia gravis?

- Antibodies are directed against nAChR on postsynaptic membrane of skeletal muscle

- Loss of functional nAChR by complement mediated lysis and receptor degradation

- End plate potentials are reduced in amplitude leading to muscle weakness and fatigue


What is a miniature end-plate potential?

- Spontaneous release of 1 vesicle therefore releasing Ach

- Doesn't reach threshold so an action potential is not activated


How is Myasthenia Gravis diagnosed?

- Measure miniature end plate potential as it shows receptor deficiency

(not enough receptors to be activated to generate a big enough enough potential by calcium influx)

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