Talk:Inward-rectifier potassium ion channel

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In mammalian neurons and muscle cells, inwardly-rectifying K-channels still pass current in the OUTWARD direction (i.e. potassium leaves the cell), causing a hyperpolarization. Although this goes against the rectification of the channel, that is still the direction of the current. The article is misleading when the channel is described as depolarizing the cell. 129.81.180.226 (talk) 22:40, 18 February 2008 (UTC)Anon

I do not believe the above description of inward rectifing pootassium channel is correct. The correct one is this: when a cell potential enters hypopolirization (the potential is more negative then its resting potential), there are 'inward potassium rectifiers' that allow K to enter the cell making the cells potential more positive and bringing it to its normal resting potential.

The description in the article is correct. Kir channels can also mediate depolarizing currents in the situation you allude to (though you might want to learn to spell), but it's important to not give people the impression that Kir channels mediate the K+ mediated repolarization current following action potential initiation (mediated instead by Kv). --Dpryan 00:01, 13 November 2006 (UTC)

[edit] question

Is this sentence right?: "Thus in cells with a -60 mV resting potential, these channels would be inactivated at membrane potentials greater than -40 mV."

I thought that they close - that means that they were blocked by spermine or mg2+ - at -70 mV. -70 mV is +20 mV over the K+-equilibrium potential of -90 mV. At -90 mV the flux of K+ is zero and when the flux of k + is getting more , mg2+ or spermine is carried along into the channel and the channel is blocked. But at a resting potential of -60 mV the conductance of Na+ is such high that on the other side the conductance of K+ out of the cell is high, too. That means that at a resting potential of -60 mV is not achieved.

Well thats what I found on other sites in the internet....is that right? 80.144.202.70

I've reworded that sentence to be less confusing. What I assume the original author (wasn't me) meant was that for a K+ reversal potential of -60mV then Kir channels would largely be blocked at -40mV. -60mV isn't what all of us were taught to be the K reversal potential, but it can happen, for example, in muscle. Of course, this is all a generalization since some Kir channels are only weakly rectifying (e.g., Kir1 family) and could still conduct significant current at more depolarized potentials...but it's probably not best to deluge the reader so early on with such details. BTW, you may want to be more careful with the usage of the word "close". I, and likely others, consider "plugged" channels to be blocked, not closed. Kir channels can also close and this process doesn't depend on voltage or intracellular polyvalent cations...but of course that's pretty nit-picky. --Dpryan 19:06, 20 March 2007 (UTC)

[edit] new question

hi, it's me again...on some webpages you can read that there are kir-channels in neurons with a resting potential of -70 mV. Is that right?, because I always thought that the resting potentials of neurons (-70 mV) is determined by a flux of Na+ - Ions in the 'background' and that this flux is responsible for the higher resting potential. The Na+ - flux results in a K+ - flux out of the cell, too, but that would mean that the kir-channels are blocked at this resting potential. But with blocked K+ - channels there is no resting potential possible. I hope you know what I mean. or is there a difference between weakly ones and the 'normal' ones? I didn't find more information about kir-channels in neurons on the internet, so i ask you and hope that you know a answer to my little problem. 80.144.218.94

You're over-simplifying the makeup of the membrane. Remember that there are transporters (perhaps this is what you meant by background) and chloride channels in the membrane as well. It's safe to say that sodium channels contribute only a negligible amount to the resting potential (RMP) of a normal neuron (though in some diseases this may not be the case). Of course, at more depolarized potentials the contribution of Kir channels to the RMP is decreased markedly, but there is still a small contribution. At these potentials the importance of the Cl- reversal potential is increased. Always keep in mind that there are a lot of different kinds of channels and transporters in the membrane and that it's the contribution of all of these that results in the RMP.
On a related note, you can observe a wide range of RMPs in different tissues. I've seen -30mV RMPs in spastic smooth muscle.--Dpryan 18:30, 23 March 2007 (UTC)