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

ESA 2 > M&R 5.1 - Cellular Response to Action Potentials > Flashcards

Flashcards in M&R 5.1 - Cellular Response to Action Potentials Deck (17):
1

How do action potentials open vg Ca2+ channels?

- Depolarisation = opening

- Ca2+ influx inwards due to large concentration gradient

2

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

3

Describe the diversity of vg Ca2+ channels

- Very diverse

- Found in skeletal muscle, neurones, lungs etc.

- L types are clinically relevant

4

Why are L-type vg channels clinically relevant?

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

5

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

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

6

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

Quickly breaks down Acetylcholine

7

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

8

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

9

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

10

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

11

Describe the structure of a nicotinic Ach receptor

- 2 alpha subunits

- 5 subunits

- Binds 2 molecules of Ach to cause a conformational change

12

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

13

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

14

What is Myasthenia Gravis? How does it present?

- An autoimmune disease targeting nAch receptors

- Profound weakness that increases with exercise

15

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

16

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

17

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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