Session 5 ILOs - Action Potential and NMJ Flashcards
Describe the 4 properties of the action potential
- Is a change in voltage across the membrane
- Depends on ionic gradients and the moments of ions across the membrane
- All or nothing (threshold)
- Propagated without the loss of amplitude
Explain the ionic basis of the action potential
- At resting membrane potential (set close to the equilibrium potential for K+, maintained by the Na+/K+ ATPase)
- Rapid depolarising phase (caused by the rapid influx of Na+ due to increased Na+ conductance and channels opening)
- Repolarising phase (caused by efflux of K+ due to closing of Na+ channels and opening of K+ channel)
- Hyperpolarisation (overshoot caused by the over-efflux of K+ leaving the cell due to prolonged opening of the K+ channels)
- Correction back to resting membrane potential (occurs through Na+/K+ ATPase which resets by bringing 2K+ in and kicking 3Na+ out)
Explain how the ionic permeability of the membrane alters with time
Initially, there is low permeability to Na+ and K+ due to charged nature of the ions being unable to cross the membrane and Na+/K+ ATPase being the only method
On initiation, Na+ permeability greatly increases (Na+ flood in)
However, Na+ channels inactivate and close and the K+ permeability increases causing an efflux of K+
The K+ permeability then decreases, but slowly, leading to the hyperpolarisation overshoot (corrected by NA+/K+ ATPase)
Describe some molecular properties of:
- Voltage gated Na+ channels
- Voltage gated K+ channels
- Voltage gated Na+ channels
- Channel is up of 1 alpha subunit, which contains of 4 similar sections or repeats (which form the channel) each made up of 6 transmembrane domains
- Voltage sensor is on S4
- Has an inactivation pore between 3-4
- Has a central pore - Voltage gated K+ channels
- Channel is up of 4 individual alpha subunits, each made up of 6 transmembrane domains - need 4 individual units to come together
- Voltage sensor is on S4
- Does NOT have an inactivation pore
- Has a central pore
Explain how local anaesthetics have their effects
Local anaesthetics block the initiation and propagation of action potentials by preventing the voltage-dependent increase in Na + conductance.
It is primarily the ionised form that binds to the channel and blocks it. Many local anaesthetics bind most strongly to the inactivated state of the channel. Therefore, at any given membrane potential, the equilibrium between resting and inactivated channels will, in the presence of a local anaesthetic, be shifted in favour of the inactivated state
- Unprotonated (lipophilic) - not use dependent
- Protonated (hydrophilic) - use dependent (only works if the channels are open)
Outline the steps of the action potential
- Begins at resting membrane potential
- Rapid depolarising phase
- Repolarising phase
- Hyperpolarisation (overshoot)
- Correction back to resting membrane potential
Recall the resting membrane potential in:
- An axon
- Skeletal muscle
- Smooth muscle cells
- Cardiac myocytes
- SA Node
- An axon = -70mV
- Skeletal muscle = -90mV
- Smooth muscle cells = -50mV
- Cardiac myocytes = -80mV
- SA Node = -90mV
Describe how conduction velocity can be measured
Conduction velocity of the action potential is determined by measuring the distance travelled (length of the nerve in m) and dividing by the time (sec) taken to complete the reflex arc
Conduction velocity = distance (m) / time (sec)
Explain the local circuit theory of propagation
Upon a depolarising current, the positive ions will repel any other positive ions in the vicinity and attract negative ions in the vicinity (local current).
However, the depolarisation will decrease the further away you are from the the point of current infection
Explain how conduction velocity is linked to fibre diameter
Axon diameter is directly proportional to conduction velocity.
Larger diameter axons have a higher conduction velocity, which means they are able to send signals faster. This is because there is less resistance facing the ion flow
Explain the implications of myelination for conduction
The myelin sheath functions to electrically insulate the axon.
Myelination increases the rate of conduction, as it forms the nodes of Ranvier (excitable axonal membrane is exposed to the extracellular space only at the nodes of Ranvier), which then allows the propagation to ‘jump’ increasing the speed at which the signal can be propagated
Describe certain consequences of demyelination
A loss of myelin with relative preservation of axons, results from diseases that damage myelin sheaths or the cells that form them.
Demyelination slows down messages sent along axons and causes the axon to deteriorate.
Example: Multiple sclerosis
Explain how action potentials open Ca2+ channels
Arrival of an action potential depolarises a membrane causing the voltage to change, which triggers the opening of voltage-gated calcium channels and influx of calcium
Describe some aspects of Ca2+ channel diversity and function
The structure of Ca2+ channels is very similar to Na+ (1 alpha subunit with 4 repeat subunits)
Different isoforms exist that represent different types in different locations in the body:
e. g. L-type calcium channels in the muscles, neurones, lungs
e. g. P/Q typecalcium channels in the neurones
Describe events leading to transmitter release (including snare proteins)
- Depolarisation arrives at the pre-synaptic junction
- Depolarisation causes the voltage to change, which triggers the opening of voltage-gated calcium channels - Subsequent influx of calcium
- Calcium binds to the synaptotagmin and the vesicle is brought close to the membrane
- The snare complex makes a fusion pore
- Neurotransmitters are released through this pore
