Matt Jones wrote in message <782jvb$l8l$1 at fremont.ohsu.edu>...
<snip a lot of detail>
>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.
I like to think of the Hodgkin-Huxley mechanism, the basic
voltage-controlled sodium and potassium channels as the
basic foundation, the "cake". On top of that you can put the
"icing" -- all the special details of Ca channels and Ca
controlled K channels, and all the rest.
It is amazing to discover how many different types of cells are
decorated in so many spectacular ways with different types of
icing, each contributing in some special way to the special
mode of operation of that cell. Herein lies the fallacy of the
computer types who would "simulate the brain" with rather
simple-minded neuron models. (I am not referring to the
computational neuroscientists who try as accurately as
possible to model the "icing" as a means to understand
it).
