module 7- action potentials

knock on mechanism in potassium voltage-gated channels

1. selectivity filter strips hydration shell from ion → ion moved into channel

2. the entry of one 1 K ion into the channel pushes one of the other ions occupying the channel out of the other side

   • oxygen atoms help stabilise the ion as it passes through the membrane (because potassium ions are the right size for interaction)

when do sodium voltage-gated channels innactivate

1msec after membrane potential reaches the threshold (action potential)

how does sodium voltage-gated channel open during depolarisation

voltage sensor moves & pulls the channel open

inactivation gate in sodium voltage-gated channels

• found between 3rd & 4th psuedosubunits

• ball & chain like structure on sodium voltage-gated channels swing up & blocks the gate which causes channel inactivation (no more Na ions can leave cell)

duration of action potential in neurones

2 msecs

duration of action potential in skeletal muscle

5 msecs

duration of action potential in the heart

200 msecs

anatomy of an action potential (draw)

Na voltage-gated channels at resting potential

probability of closing >> probability of opening

Na voltage-gated channels at below threshold stimulus

probability of closing > probability of opening

Na voltage-gated channels at above threshold stimulus (depolarisation)

probability of closing << probability of opening

what is dravet syndrome

• form of epilepsy

• inheritable

• mutation of SCN1A gene that codes for a sodium channel → mutation prevents action potentials in inhibitory neurons so lack of inhibition in some brain regions

• Na_v1.1 is mutated → main sodium channel expressed in inhibitory neurons

how can dravet syndrome be treated

• cannabinoids (CBD)

• NICE guidelines → since 2019 its been legal to prescribe cannabinoids for treatment resistant epilepsies

what does the relative refractory period prevent

prevents action potential from spreading backwards across axon