IUBio

question on ACTION POTENTIALS!

Matt Jones jonesmat at ohsu.edu
Mon Jan 18 14:43:14 EST 1999


In article
<Pine.GSO.3.96L.990118042608.14751B-100000 at unixs3.cis.pitt.edu> Mohanraj
Narayanan, monst3+ at pitt.edu writes:
>After the Na+ ions migrate into the cell in response to depolarization, I
>was told that the ca2+ ions enter the cell so as to make K+ ions migrate
>out of the cell to bring the voltage down. I was also told that the
>sodium-potasium pump kicks in and removes the Na+ to bring down the
>voltage to resting potential.  I am confused. Why does the ca2+ come in if
>all the cell had to do was pump out the Na+ ions with the Na+/K+ pump? 
>
>also, I am confused on the details of why there is a short
>hyperpolarization just after the voltage comes back down to resting
>potential.
>
>any input would be greatly appriciated.
>thank you 
>

I can understand the confusion. Here's how it works:

There are a bunch of ion channels that form pores through which ions can
move across the membrane. Most of the ones that concern us in this
discussion are "voltage-gated ion channels", which means that they are
normally closed at the cells resting potential, but they can open when
the membrane is depolarized. Let's just confine ourselves to the
voltage-gated Na+ and K+ channels for now.  You probably know that
there's a lot of Na+ ions outside the cell, and a lot of K+ ions inside.
This comes about by the action of the Na+/K+ pump that you mentioned, but
other than that, we can forget about that pump altogether when discussing
the action potential. Just remember that you need it to set up the ionic
gradients. It is NOT required for repolarization after an action
potential, it just sets up the ionic gradients (whoever told you that
should stop telling people that). 

These gradients produce a resting potential because the membrane is
normally selectively permeable to K+ ions (i.e., there are a few pores
that pass K+, which are open all the time). Because there's a lot of K+
inside and not much outside, there is a chemical gradient that tends to
drive K+ out of the cell. However, each K+ ion that leaves changes the
potential of the inside of the cell by a small amount (in the negative
direction). At some point, the chemical drive of K+ out of the cell is
exactly balanced by the electrical attraction of K+ to the negative
potential inside. This balance point is called the potassium equilibrium
potential, and in the simplest possible world is identical to the cells
resting potential (-90 mV, lets say). At the equilibrium potential,
there's no NET movement of K+, because the inward and outward forces are
exactly balanced.

Right. Now let's suppose the membrane is depolarized a little bit (by a
synaptic input, or current injected through a recording electrode, or
whatever). Some of the Na+ channels will open in response to this
depolarization, letting Na+ ions flow into the cell.  It doesn't really
matter how many Na+ ions come in. What really matters is that the
membrane has now become slightly more permeable to Na+. The membrane
potential will now depolarize a little more to try to attain a sort of
weighted average of the equilibrium potential for K+ and for Na+ (the Na+
equilibrium is way way positive). The trick is that the channels that let
in the Na+ are themselves sensitive to depolarization, so a few more of
them open, increasing the Na+ permeability, depolarizing further, opening
more channels, increasing the Na+ permeability, depolarizing further,
etc... This is a "regenerative" process, and we call it an action
potential or a spike ('cause that's what it looks like on an
oscilloscope). The potential at which the amount of Na+ conductance is
just enough to begin this regenerative spike is called the "spike
threshold".

Meanwhile, the depolarization is also causing K+ channels to open. But
these channels are relatively sluggish in their response to potential,
usually having a sizable delay between the time the potential changes and
the time they open (they are called "delayed rectifiers", which means
that they open slowly in response to depolarization, and close upon
hyperpolarization). So AFTER the spike has already started up, these
channels open up and increase the K+ permeability, which tends to bring
the potential back down. 

The final item we need (which I have put off until last because it's a
bit confusing) is a thing called "inactivation" that happens to Na+
channels. At the peak of the spike, we have a situation in which both the
Na+ and K+ channels are all pretty much open. If we just left it like
this, then the membrane would take on some weighted average of the two
equilibrium potentials, and would end up just sitting at around 0 mV. But
that's not what really happens. Instead, as you know, it quickly drops
back down to rest. The reason for this is that Na+ channels don't stay
open indefinitely when they're depolarized. The "inactivate", meaning
that they close even while depolarized, and stay closed until they can be
reprimed by hyperpolarization. So, soon after the peak of the spike, the
Na+ channels inactivate, leaving a huge permeability to K+, which drags
the membrane back down to -90.  Again, the pumps are NOT necessary to
repolarize the membrane after a spike (but the whole machine will
eventually stop working without the pumps to set up the gradients).
Inactivation also means that there will be a short period AFTER the spike
is over during which further stimulation won't cause another spike,
because the Na+ channels are still inactivated and haven't had time to
recover. This period is called an "absolute refractory period", and
you'll read about it in your textbook.

As far as Ca++ coming in and turning on K+ channels, well, yes that can
also happen (it doesn't have to), but you don't need to worry about that
to understand how action potentials work. Briefly, there are
voltage-gated Ca++ channels that open when the cell is depolarized. They
help to generate spikes sort of like the Na+ channels do, and they also
let in Ca++ which causes some special effects in cells, including turning
on a class of K+ channels called, you guessed it, calcium-activated K+
channels. These are not the same channels as the delayed rectifiers, but
since they're K+ channels that respond to depolarization (and Ca++), they
pretty much do similar things.

So that's it.

Cheers,

Matt Jones



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