Action Potentials and Neuromuscular Junctions Flashcards

1
Q

What is an Action Potential

A

Change in voltage across the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the properties of an Action Potential?

A
  • Depends on ionic gradients and relative permeability
  • Only occur if a Threshold Level is reached
  • Propagated without Loss of amplitude
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the Threshold Potential

A

The minimum membrane potential that must be reached for an Action Potential to be generated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens during Repolarisation?

A
  • Na channels inactivate, Na stops moving in
  • K channels open, K moves out
  • Na Pump is NOT involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Compare Absolute and Relative Refractory Period

A

Absolute: Nearly all Na channels inactivated so no AP can be generated

Relative: Na channels recovering from inactivation, More Na channels becoming activated, AP can be generated from a large enough stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Compare voltage gated Na and K channels.

A

Na:
- 1 Channel= 1 Alpha subunit= Central pore surrounded by 4 repeats. (Similar to Ca Channel)

K:
1 Channel= 4 Alpha subunits around a Central pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do local anaesthetics bind and block Na channels?

A
  • Most are weak bases and cross membrane in unionised form
  • Block open Na channels easily
  • Higher Affinity for inactivated Na Channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In what order do local anaesthetics block nerve fibre conduction?

A
  • Small myelinated neurons
  • Non myelinated neurons
  • Large myelinated neurons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to calculate Conduction Velocity?

A

Distance travelled by impulse/ time taken

In m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What axon properties lead to a high Conduction Velocity?

A
  • Low Membrane Capacitance (Cm)
  • High Membrane Resistance (Rm)
  • Large Diameter ( Lower Axon Resistance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Capacitance, Cm?

How does it affect conduction velocity

A
  • Ability of a Lipid bilayer to store charge

High Cm means more charge stored, so Decreased spread of Local Current, so Decreased Conduction Velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Membrane Resistance, Rm?

How does it affect conduction velocity?

A
  • A function of open ion channels

High Rm means less open ion channels, means less Local Current Loss ( Less leakage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the Local Circuit Theory

A

Depolarisation of a small region of membrane, produced local currents which depolarise adjacent regions, caused voltage gated Na channels to open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the relationship between Diamter and Conduction Velocity for Myelinated and Non-Myelinated neurons?

A

Non-myelinated: Velocity is proportional to Diameter^0.5

Myelinated: Velocity is proportional to Diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does Saltatory Conduction work?

A

Action Potential jumps from one Node of Ranvier to another and so on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why don’t Action Potentials move backwards?

A

Channels that have been opened, are now in Refractory Period so are inactivated

17
Q

How does myelin sheath affect conduction velocity?

A

Reduced Cm, Increased Rm

= Increased Conduction Velocity

18
Q

What are some properties of voltage gated Ca Channels?

A
  • Similar to Na Channel
  • Various channel types
  • Ca channels activate/ inactivate slower than Na Channels
  • High intracellular [Ca] leads to channel inactivation
19
Q

Explain the process of Transmitter release

A
  1. Ca enters cell
  2. Binds to a protein, which brings vesicle to membrane
  3. Snare complex makes fusion pore in vesicle
  4. Transmitter is released through pore
  5. Transmitter degraded
20
Q

How do Competitive and Depolarizing Neuromuscular Blockers work?

Give an example of Depolarizing

A
  1. Competitive: Occupy receptors so transmitter can’t bind
  2. Depolarising: Maintain depolarisation In Muscle end-plate, so inactivated Na channels do not activate, and no Na enters cell (E.g. Succylincholine)
21
Q

Where are Neuromuscular blockers used and why?

A

In surgery, causing temporary paralysis to relax muscles

Someone paralysed like this can’t move/ speak but WILL FEEL PAIN

22
Q

What is Myasthenia Gravis, how does it work?

A
  • Autoimmune disease targeting nAChRs
  • Antibodies target nAChRs on muscle end-plate
  • Receptor degradation leads to loss of functioning nAChRs
  • Reduced amplitude of Potentials at end-plate (threshold not reached)
23
Q

What are some symptoms of Myasthenia Gravis

A
  • Muscle weakness and fatigue
  • Weakness increases with exercise
  • Double vision
  • Drooping eyelids