IUBio

question on ACTION POTENTIALS!

Matt Jones jonesmat at ohsu.edu
Tue Jan 19 13:47:07 EST 1999


In article <36A438FA.167E at afmb.cnrs-mrs.fr> Eric Blanc,
eric at afmb.cnrs-mrs.fr writes:
>That's not the end of the action potential.
>AP terminates with an hyperpolarization phase, which results from the
>opening of calcium activated potassium channels. Large-conductance
>calcium activated potassium channels are responsible for the fast
>after-hyperpolarization phase, and small-conductance calcium-activated
>potassium channels are responsible for the slow AHP.
>
>Why is it so rare to talk about this last process ?
>
>Moreover, nerve fibers are myelinidated in vertebrates. Action
>potentials are not continuous all along the fiber, but jump from one
>node to another.
>To further complicate  this model, potassium channels are absent from
>the nodes.
>Action potentials are faster and more efficient, due to these reasons.
>But Neuronal action potentials are somewhat different from those evoked
>above.
>Really tricky.

Regarding the after hyperpolarization: In my previous post, I set up a
"simplest possible" scenario, in which the resting potential was exactly
the same as the K+ equilibrium potential. Richard Norman correctly
explained that this is not really the case: the resting potential is
approximately a weighted average of the various equilibrium potentials
for all the ionic conductances that are open at rest. This won't be
exactly E-K+, because there are also resting Na+, Cl- and other leak
conductances, so rather than -90 mV, neurons tend to rest around -60 to
-80 mV. However, during the action potential, a lot more voltage-gated K+
channels are opened by depolarization than are open at rest. Even without
the contribution of Ca++ -activated K+ channels, this additional K+
conductance is sufficient to temporarily shift the cell's overall
equilibrium potential closer to that of K+ (-90 mV, say). Thus, after Na+
channels close, the cell temporarily seeks a new "resting" potential more
negative than the true resting potential, and thus undershoots rest until
the extra K+ channels close. This is the immediate basis of the
afterhyperpolarization. NOT necessarily the recruitment of Ca++-activated
K+ channels, just the extra voltage-gated K+ channels recruited during
the spike.

Having said that, I reiterate that in some cells, there is an involvement
of Ca++-activated K+ channels in repolarization and/or long lasting AHPs,
but this is not necessary just to get an AHP. I don't know if squid axon
has Ca+-Acitvated K+ channels, and certainly Hodgkin and Huxley did not
include them in their simulations, which afterhyperpolarize just fine
anyway. Also, 4-AP can increase spike amplitude and duration in
myelinated axons, suggesting that there _are_ K+ channels in or near the
nodes, and there is immunohistological evidence of this also, at least
under some conditions.

In intact central neuronal circuits, by the way, there an awful lot of
things that generate afterhyperpolarizations, including recurrent
inhibitory synaptic feedback. I believe that part of the "reason" for
this is to more effectively remove inactivation of Na+ and Ca++ channels,
so as to allow more rapid or more complex spike firing. A great example
of this is in thalamic oscillations, in which GABA-mediated IPSPs
_promote_ "rebound" spike firing by repriming T-type Ca++ channels.

Cheers,

Matt Jones



More information about the Neur-sci mailing list

Send comments to us at biosci-help [At] net.bio.net