Action Potentials and Neuromuscular Junctions Flashcards
What is an Action Potential
Change in voltage across the cell membrane
What are the properties of an Action Potential?
- Depends on ionic gradients and relative permeability
- Only occur if a Threshold Level is reached
- Propagated without Loss of amplitude
What is the Threshold Potential
The minimum membrane potential that must be reached for an Action Potential to be generated
What happens during Repolarisation?
- Na channels inactivate, Na stops moving in
- K channels open, K moves out
- Na Pump is NOT involved
Compare Absolute and Relative Refractory Period
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
Compare voltage gated Na and K channels.
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 do local anaesthetics bind and block Na channels?
- Most are weak bases and cross membrane in unionised form
- Block open Na channels easily
- Higher Affinity for inactivated Na Channels
In what order do local anaesthetics block nerve fibre conduction?
- Small myelinated neurons
- Non myelinated neurons
- Large myelinated neurons
How to calculate Conduction Velocity?
Distance travelled by impulse/ time taken
In m/s
What axon properties lead to a high Conduction Velocity?
- Low Membrane Capacitance (Cm)
- High Membrane Resistance (Rm)
- Large Diameter ( Lower Axon Resistance)
What is Capacitance, Cm?
How does it affect conduction velocity
- Ability of a Lipid bilayer to store charge
High Cm means more charge stored, so Decreased spread of Local Current, so Decreased Conduction Velocity
What is Membrane Resistance, Rm?
How does it affect conduction velocity?
- A function of open ion channels
High Rm means less open ion channels, means less Local Current Loss ( Less leakage)
Describe the Local Circuit Theory
Depolarisation of a small region of membrane, produced local currents which depolarise adjacent regions, caused voltage gated Na channels to open.
What is the relationship between Diamter and Conduction Velocity for Myelinated and Non-Myelinated neurons?
Non-myelinated: Velocity is proportional to Diameter^0.5
Myelinated: Velocity is proportional to Diameter
How does Saltatory Conduction work?
Action Potential jumps from one Node of Ranvier to another and so on
Why don’t Action Potentials move backwards?
Channels that have been opened, are now in Refractory Period so are inactivated
How does myelin sheath affect conduction velocity?
Reduced Cm, Increased Rm
= Increased Conduction Velocity
What are some properties of voltage gated Ca Channels?
- Similar to Na Channel
- Various channel types
- Ca channels activate/ inactivate slower than Na Channels
- High intracellular [Ca] leads to channel inactivation
Explain the process of Transmitter release
- Ca enters cell
- Binds to a protein, which brings vesicle to membrane
- Snare complex makes fusion pore in vesicle
- Transmitter is released through pore
- Transmitter degraded
How do Competitive and Depolarizing Neuromuscular Blockers work?
Give an example of Depolarizing
- Competitive: Occupy receptors so transmitter can’t bind
- Depolarising: Maintain depolarisation In Muscle end-plate, so inactivated Na channels do not activate, and no Na enters cell (E.g. Succylincholine)
Where are Neuromuscular blockers used and why?
In surgery, causing temporary paralysis to relax muscles
Someone paralysed like this can’t move/ speak but WILL FEEL PAIN
What is Myasthenia Gravis, how does it work?
- 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)
What are some symptoms of Myasthenia Gravis
- Muscle weakness and fatigue
- Weakness increases with exercise
- Double vision
- Drooping eyelids
