h2g2 The Hitchhiker's Guide to the Galaxy: Earth Edition

I'm studying the chemistry of the nervous system, and one thing I've found is that transmitting a signal along a nerve cell involves changing the voltage across the cell membrane by letting sodium ions into the cell, and then restoring voltage by letting potassium ions out.

Now, all the books I've looked up say that the opening of both the sodium and potassium channels is caused by membrane depolarisation; however, the opening of the potassium channels is delayed by a few milliseconds to give the sodium channels time to work. Unfortunately, they don't say what causes this delay. Google and Scirus both turn up nothing useful.

So, here's the question - is the cause/mechanism of this delay known, or is it an unsolved mystery?

Traveller in Time not a chemist, nor biologist, familiar with the subject
"Can you have a little time for the 'chemical reaction' to take place ? The depolarisation is a chemical process after all. "

I would imagine (note vague disclaimer... It's about 14 years since I studied electrophysiology in the very first term of my degree!) that it represents a physical difference in the way that the channels respond to changes in voltage. As the potential increases, sodium channels open; as it increases further, they close and potassium channels open. Perhaps the difference in the amino-acid composition of the channels (i.e. positive and negatively charged residues) affects the potential at which the physical changes occur that lead to opening and closing of the channels..?

*sits back and waits to be proved wrong*

http://www.blackwellpublishing.com/matthews/neurotrans.swf
has some pretty piccies.
Would appear there is more going on than just a neuro transmaitter opening the channel and the various ions flowing through it.

I just googled 'delayed neuronal release of potassium' and got a shed load of hits. There's plenty out there but it's way beyond me at the moment!

Those images relate to neurotransmitter-triggered initiation of action potentials at synapses, whereas I think (again, willing to be proved wrong!) that the original question related to the voltage-gated channels that propagate action potentials after they're initiated.

I'm hoping Chris comes across this cos I think it is area they know about (but may be wrong inthat assumption).

I think the original question is conflating and confuses a much more complicated process. The propogation of action potentials along the axon (nopt the cell body) is an electric signal and there's no ingress or egress of ions to/from the axon. However the action potential, which is initiated at the axon hillock, is initiated by internal chemical reactions in the cell body which are in turn initiated by the ingress and egress of ions through the cell membrane which requires neurotransmitters to open the channels.

But I also am operating at the limits of my knowledge!

"The propogation of action potentials along the axon (not the cell body) is an electric signal and there's no ingress or egress of ions to/from the axon."

I may have been carrying round completely false information for 14 years (wouldn't be the first time...), but I understood that an action potential is the changes in membrane conductance along the length of the axon, not an electrical current passing along the axon. The axon membrane normally exists at a resting potential of -90mv. When a signal is received, the sudden opening of sodium channels allows sodium ions to flood into the axon, which depolarises the membrane to a potential of +35 mV. After a delay (the subject of the original question), voltage-gated potassium channels open, allowing potassium to flood out of the axon, causing repolarisation back to the resting state. This process occurs sequentially along the length of the axon - depolarisation in one region causes voltage-gated sodium channels in neighbouring regions to open - and the signal is transmitted. When it reaches the end of the axon, the depolarisation of the membrane triggers the release of neurotransmitter and the action potential is passed on to the next neuron or to an end organ (e.g. skeletal muscle).

Have I completely missed the point..?

your use of exact voltages and indepth description of the process would indicate you are being kind to me
I certainly can;t compete with that level detail so I would say it is most likely myself that is getting confused!

Don't count on it! All this was thrown at us in our first term at medical school and I never really got to grips with it. I think I just have a mental block when it comes to electricity - I could never really grasp circuits and Kirchoff's Laws and all that nonsense at school, either This is probably why I ended up in genetics - the only electrical currents involved are the ones that happen when you press the 'on' button on whichever piece of equipment you happen to be using...

Anyway, to get back to the question, it would be nice if someone who *really* knows what they're talking about could stop by and give us an answer, rather than the two of us sitting here cheerfully speculating

It does having something of the air of 'pub expert' about it doesn;t it

Traveller in Time electronics engineer
"There is no machanical switch acting in no-time. Even electronics have to build up a saturation for nano seconds.

What I hear it is more like a zenerdiode curve then a switch. "

A nerve signal is less like an electrical current, but more like a chain-reaction of ion channel openings sweeping up the length of the nerve cell.

Potassium channel opening happens after membrane depolarisation to return the axon to resting potential. Hence their name "delayed rectifier potassium channels". It's an in-built part of the mechanism without which the action potential would be a one-off thing for the nerve cell.

As for the actual mechanism (speculation on my behalf here) - it is likely bought about by a difference in protein shape of the channel itself - when the channel (a complex of proteins) opens, it deforms. It is unlikely that two channels with two functions (sodium and potassium ion transport, respectively) deform at the same precise instant. The lag in potassium channel opening was coopted by evolution for this function.

Ste

Yeah - that's what I meant

(No, honestly, it was, but Ste has phrased it far more concisely and clearly than I did )

Ah, I see. Well, even if no one else has, I've learnt something today Which is what it is all about after all.

You gotta love google.

Cheat! And there was me confronting the demons of my youth and sifting through 1100 pages of 'Principles of Neural Science'

Well... I had an idea and just did some fact-checking. The channel deformation was just speculation on my behalf too...

You might also like to look up the Hodgkin-Huxley model if differential equations don't scare you off.

Right...just so I'm clear, you're saying that potassium channels simply open more slowly than sodium channels (due to different amino acid sequences or some such)?