question related to neuron spiking
xli6 at gmu.edu
Fri Mar 26 10:48:17 EST 2004
Thank you very much. I am very excited. I have never realized the neuron
spiking shape is containing so many secrets, e.g. Ih, Ik(ca), ...
As you said, the afterhyperpolarization curve is from the peak of action
potential to the most hyperpolarized point and continue to the point
Vmem back to Vrest (if no after-depolarization happening here, so it
doesn't even include ADP part curve), how can we fit the curve to say it
is mono-phasic or bi-phasic?
Yes. I learned Hodgkin-Huxley model from the book. But in the world many
people are talking about Ca++ activated K+ channel in the neuron
spiking. In a neuron spiking, is K(Ca) channel actually playing more
role than the classical HH K channel? Is the classical HH K channel
actually not common in the real world? I am interested in seeing a slow
AHP caused by K(Ca).
Actually I am not aware that by studying the shape of neuron spiking,
one can find out its underneath mechanism. In my impression, almost no
any textbook emphasized this part. Hille's, Kandel's, Johnston's,...
I think it would be great somebody write this part. Or if you could
point me more sources?
Thank you very much. I greatly appreciate it.
Matt Jones wrote:
> Yes, you did know that phenomenon. But that isn't what peole mean by
> ADP. They mean that after a spike, the cell becomes transiently
> *depolarized* compared to rest.
> There are a lot of ways that you can change the HH model to get this
> to happen. One way (I predict, but haven't actually modeled) is to
> adjust the balance of Na- and K-channel gating constants and reversal
> potentials so that the AHP is very deep, the Na-channel activation
> curve starts to rise near the resting potential, and the Na-channel
> inactivation curve is very steep. This would allow the AHP to
> "deinactivate" a lot of Na-channels, so that they would actually begin
> to reopen during the falling phase of the AHP, slightly depolarizing
> the cell (but you'd have to balance the rate constants just right in
> order to avoid always getting a second spike).
> The HH equations are somewhat oscillatory in the subthreshold regime,
> and the type of ADP described above is a manifestation of that
> However, that's not what most people mean by ADP. Most people mean
> that there is a *new depolarizing conductance* that is somehow opened
> after a spike. Again, there are several ways to get this to happen.
> One way is to have a *hyperpolarization-activated cation current*, for
> example the "H" current Ih. This current is not part of the original
> HH equations, but one can easily add it to an HH system by taking
> their Na-channel model and rearranging the voltage-dependence and
> gating constants.
> If Ih is present, then the AHP will turn it on, and it in turn will
> depolarize the cell causing an ADP. If Ih is sufficiently strong, it
> will lead to secondary spikes, possibly accounting for the doublet or
> burst firing that the paper refers to. This sort of current is
> important in a lot of pacemaker systems, such as the heart, and also
> lots of neurons that show oscillatory tendencies, such as stellate
> cells in entorhinal cortex.
> As for biphasic AHPs, people are refering to how many components exist
> in the decay phase. Again, the simplest way to get a biphasic AHP is
> to *add* a new K-channel with different kinetics. For example, some
> common very long-lasting AHPs are caused by calcium-activated
> K-channels. These are long lasting (100s of ms) because calcium (which
> came in during the spike) has to be cleared by pumps or buffering
> proteins before the current will turn off. Their are probably also
> calcium-activated cation channels that could cause long ADPs.
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