The Student Room Group
Reply 1
DartsOfPleasure
Ok, I understand that there is an absolute refractory period and then the relative refractory period after an action potential has been generated. But what exactly is happening to the sodium channels in these two periods? Are the open/closed? Why cannot another impulse be generated during the absolute period?

Thanks


During the absolute refractory period the sodium channels are either already open or in their inactivated state, hence no depolarisation can occur (since it requires an influx of sodium thru these channels).

The relative refractory period coincides roughly with the period of hyperpolarisation (i.e. when there is a large efflux of potassium ions beyond what is needed to bring the membrane potential back to normal). During this stage, some of the voltage sensitive sodium channels have returned back to their resting state. However, since the cell is hyperpolarised, a larger than usual stimulus is required to reach the threshold potential and cause an action potential.

Does that help?
Reply 2
I have a couple of questions about this...

1) What exactly happens to sodium channels when they "inactivate"?

2) Why do local anasthetics work better on inactivated sodium channels?

And happy new year biology forum people... Good luck recovering from hangovers... lol...
Reply 3
Revenged
I have a couple of questions about this...

1) What exactly happens to sodium channels when they "inactivate"?

2) Why do local anasthetics work better on inactivated sodium channels?

And happy new year biology forum people... Good luck recovering from hangovers... lol...


1) Sodium channels have an additional intracellular structure, called the inactivation gate, which blocks the channel shortly after it opens, hence limiting the influx of sodium. When the cell is repolarised, the closure of the sodium channels forces the gate back out of the channel.

2) This answer probably sounds pretty dumb, but the reason why they work better on inactivated sodium channels is because local anaesthetic molecules have a much higher affinity for inactivated than for resting channels. I don't know why they have a higher affinity thou.
Reply 4
Thanks... So the sodium channel opens, inactivates and then closes... and this closure of the sodium channel reactivates the channel?
Reply 5
Not sure what you mean with 'reactivates'. The closure of the sodium channels puts them back to their resting states. They open up again once the threshold potential is reached.
Reply 6
Ok, that makes more sense now...
Reply 7
Hi random but i understand what the refractory period is, and that it's returning the cell membrane to it's resting potential. but what is the point of it? so another impulse can't fire straight away? is that it? because have come across this question in a past paper and can't understand what the benefit is. thanks
Reply 8
bluelou
Hi random but i understand what the refractory period is, and that it's returning the cell membrane to it's resting potential. but what is the point of it? so another impulse can't fire straight away? is that it? because have come across this question in a past paper and can't understand what the benefit is. thanks


well it ensures that impulses cannot travel backwards - ie local current can only flow in one direction.
Voltage gated sodium channels are responsible for the rising phase of the action potential (the depolarisation) The have voltage sensing S4 alpha helices in their alpha 3 subunit. When threshold is reached, this alpha helix twists and opens the channel causing sodium to enter the cell and depolarise.

After a short time ~2ms, an inactivation gate, the 'h' gate closes and prevents the channel from conducting current.

At the same time, voltage-gated potassium channels are activated and allow potassium ions to flow out of the cell causing the hyperpolarisation of the cell.

When the cell is hyperpolarised, the voltage gated sodium channels' inactivation gate opens again and the channel is reprimed, ready to be activated again.

http://physioweb.med.uvm.edu/cardiacep/images/FromRay/rep29.gif

If you look at that diagram, it shows how the conductance of sodium and potassium vary during the action potential. During the rising phase sodium conductance is high and then you get a delayed potassium conductance which causes the hyperpolarisation.

Now look at this diagram: http://www.unm.edu/~jimmy/refractory_periods.jpg

If you look at the absolute refractory period, the sodium channels have just become inactivated, so therefore cannot cause further depolarisation and no action potential can be fired. Also during this time, the potassium conductance begins to increase so inhibits the depolarisation necessary for action potential firing.

During the relative refractory period, most of the sodium channels have become reactivated and are able to open, however, the potassium conductance is still quite high so it takes a much larger stimulus to activate less voltage sensitive sodium channels and to overcome the high potassium conductance. This is why a second action potential can only be fired during the relative refractory period