Sodium and Potassium ions in water

[pioneer]

The post about the adding consciousness to the brain was getting a little long and departed from the original purpose of the post. I apologize for that. I thought I would start at the ionic level and show some basic relationships for some additional insight.

 

If you look at the metals K (potassium) and Na (sodium), the metal K is more reactive in water. What this implies is that the K+ and Na+, ions, although both with a single positive charge, are not created equal. The Na+ will tend to hold onto its metallic electron a little stronger, implying that the Na+ ion has more apparent postive charge than the K+ ion. Or the electro-magnetic forces are stronger in Na+.

 

This can be witnessed by comparing K+ and Na+ ions dissolved in water. The result are the central ions sharing the negative end of the dipole of water to form a structure called a hydration sphere.

 

Sodium has a stronger interaction with its first hydration shell than potassium, giving the latter a more flexible structure. © 2003 American Institute of Physics. @DOI: 10.1063/1.1559673#

http://www.scripps.edu/~trippm/papers/JCP-2003-118-7062.pdf

 

When the neurons place the Na+ on the surface, they are using the cation that has the most apparent postive charge and the most tightly bound water in the first hydration shell. The inside is richer in K+ with its lower apparent postive charge and its less tightly held first hydration shell. The situation that is created, are the neuron surfaces are covered with a lot of postive charge, with a relative strong first hydration shell that is relatively stable, relative to K+. The neurons repel each other's positive surfaces, but are anchored so they are not able to move relative to each other. The result is positive potential looking for ways to reduce this potential.

 

The points where the positive charge on different neurons is able to approach the closest are the synapses. This closeness indicates, this is where the positive charge repulsion will be at a minimum. But since the synapse retains a gap, this implies the positive potential is never zero. The direction of the Na+ current from axon to dendrite or axon, is reflective of the movement from higher toward lower positive potential. One can almost look at the brain as this big bundle of positive charge that is trying to find ways to discharge the potential, i.e,, into synampses.

 

The hydrations sphere of Na+ is an extension of the positive potential that is on the surfaces of the neurons. In other words, the Na+ does not exist just as isolated Na+, but as Na+ plus hydration. The value of this water is when neurotransmittors appear in the local water, but before they bind onto synapses, these chemicals have their own hydrated what that reflects their polar/nonpolar atoms in their structures. It is sort of an additional tweak at the level of the H ,that affects the surface Na+, even before the neurotransmittor binds to the membrane. Neurotransmittor may have more specificity at the synapse, but its appearance anywhere outside of neurons has an impact before it begins to bind. The cerebral spinal fluid is an extension of the surface water. As features in the core of the brain add chemicals, the positive potential gets tweaked.

 

They may be how the brain associates memory to valance. Any emotional response, often implies core region chemical input into the CSF. The bulk positive potentials of the brain, gets sort of primed to reflect the best possible way to lower the tweaked positive potential via the synapses. This can not be a random, since any neruon can absorb there chems. There needs to be specific synaptic selectivity for these chems to trigger associated memories.

[iNow]

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Some interesting thoughts. I am getting a better feel for your philosophy on this subject having read more of your posts. However, there are a few key details which I believe you are fundamentally missing, and I will do my best to explain the mechanisms actually in place without attacking your concept.

 

 

When the neurons place the Na+ on the surface, they are using the cation that has the most apparent postive charge and the most tightly bound water in the first hydration shell. The inside is richer in K+ with its lower apparent postive charge and its less tightly held first hydration shell. The situation that is created, are the neuron surfaces are covered with a lot of postive charge, with a relative strong first hydration shell that is relatively stable, relative to K+. The neurons repel each other's positive surfaces, but are anchored so they are not able to move relative to each other. The result is positive potential looking for ways to reduce this potential.

 

The neurons are not "placing" their ions at the surface. There is, in fact, a difference in potential across the membrane wall of the nerve cell, just as you imply. When the cell is at rest, the outside of the cell wall membrane has a positive charge and the inside of the membrane has a negative charge. This is called it's resting potential. It results from the differences of positively charged ions of sodium (Na) and potassium (K) to the negatively charged cytoplasm outside the cell. Additionally, it's useful to note that there are more Na ions concentrated outside of the cell and more K ions concentrated inside of the cell. This is important since, as you correctly mentioned, the "amount" of charge "expressed" by each ion is not equal.

 

Per the above, the concentrations of ions on either side of the cell wall membrane are not in equilibrium, and it has to be actively maintained. This is where the sodium-potassium pump comes into play. This pump actively transports the ions against their concentration gradients.

 

 

The points where the positive charge on different neurons is able to approach the closest are the synapses. This closeness indicates, this is where the positive charge repulsion will be at a minimum. But since the synapse retains a gap, this implies the positive potential is never zero. The direction of the Na+ current from axon to dendrite or axon, is reflective of the movement from higher toward lower positive potential.

There are actually openings in the cell membrane called sodium (Na) gates and potassium (K) gates, and it is these which allow the respective ions to cross. In very rough terms, the sodium on the outside of the cell goes to the inside, and the potassium on inside of the cell goes to the outside, causing a temporary reversal of the cell membrane potential... it changes polarity.

 

Since the sodium is on the outside, it reacts first to the propogating signal from the neighboring nerve cells. So, the sodium gates open first, and sodium floods into the cell. It is after this happens that the potassium gates respond, and potassium evacuates the cell, thus restoring the resting potentials net charges. The sodium-potassium pump then pushes the Na ions out of the cell and the K ions are pumped back into the cell, and the original distribution of those ions are restored.

 

This propogating signal is called the action potential. It actually does begin at one spot on the cell membrane, but then spreads to adjacent "sides" of the membrane and then across the synaptic cleft.

 

 

One can almost look at the brain as this big bundle of positive charge that is trying to find ways to discharge the potential, i.e,, into synampses.

 

The hydrations sphere of Na+ is an extension of the positive potential that is on the surfaces of the neurons. In other words, the Na+ does not exist just as isolated Na+, but as Na+ plus hydration. The value of this water is when neurotransmittors appear in the local water, but before they bind onto synapses, these chemicals have their own hydrated what that reflects their polar/nonpolar atoms in their structures. It is sort of an additional tweak at the level of the H ,that affects the surface Na+, even before the neurotransmittor binds to the membrane.

I suppose this is the part of your post that sounded most interesting. It seems to make logical sense. I would, however, like to see some detailed clarification, if possible, also some studies along these lines. After all, logic makes people think that heavier objects reach the ground more quicky, but empirical data proves this is not the case. Empiricism beats logic any day.

 

 

Neurotransmittor may have more specificity at the synapse, but its appearance anywhere outside of neurons has an impact before it begins to bind. The cerebral spinal fluid is an extension of the surface water. As features in the core of the brain add chemicals, the positive potential gets tweaked.

I am not familiar with the idea that neurotransmitters may carry some charge... that they are ions, but I am honestly not sure. This may, in fact, be the case, but it doesn't trigger any recall from my 4 years of study. If you are able to provide some support that NTs carry charge, then that's great, but until then I'd caution you not to carry this line of reasoning too much farther.

 

It is in the cell body of the neuron that the neurotransmitters are produced. These molecules are transported down the axon to the axon terminal, and are stored in vesicles, which are like little bundles or balloons. It is only when these vesicles "fuse" with the cell membrane of the axon terminal that they released into the synapse. What happens then is the neurotransmitters will ONLY bond with certain specific receptors on the neighboring nerve cell. It as if there are a series of locks on the neighboring nerve cell, and the neurotransmitters are keys. The key must fit the lock, or the door will not open. (Note - Nitric Oxide (NO) is not stored in vessicles, and it diffuses through the cell membrane instead of being released by fusing with the axon terminal. It then activates enzymes in the neighboring cell which produce something called "second messengers.")

 

 

They may be how the brain associates memory to valance. Any emotional response, often implies core region chemical input into the CSF. The bulk positive potentials of the brain, gets sort of primed to reflect the best possible way to lower the tweaked positive potential via the synapses. This can not be a random, since any neruon can absorb there chems. There needs to be specific synaptic selectivity for these chems to trigger associated memories.

Again... not so sure about this, but hey... I'll give it a definite maybe. It really is important that if you are going to use logic and deduction to understand a system that you are not working from a set of false premises. Houses built in sand will topple, ya dig?

 

 

In the interest of transparency, I want to state that I spent some time refreshing my knowlege of this subject by reviewing the links which I tied to many of the words within my post. I'd be glad to elucidate further on any of these points as needed, but am myself a student of life and don't hold all of the answers either.

 

 

Speculation is fun, but science is funnerer.

[pioneer]

Thanks for the extra details and clarifications. I may have mixed up neurotransmittors and the chemicals that are inputted into the cerebral spinal fluid, which become the water potential the neurons bath in.

 

Relative to neurotransmittors, the charge is usually more based on dipoles. In the image of the neurotransmittor aspartic acid there are 3 or 4hydrogen bonding hydrogen The H are induced to have a slight positive charge. Being an acid, it can also exist with a negative charged base. This is perfect for lowering positive potential. There are also some organic aspects for an additional tweak. This chemical floating in water is surrounded by water so its affect is spread out before absorption.

 

 

The idea of the brain's neuron surfaces being loaded with positive charge, that needs to lower, cuts to the heart of why we need synapses. The synapses, by allowing the positively charged surfaces of neurons to get the closest shows, this is where the positive potential is not quite as high as the bulk neurons. This is reflected in the little bulb on the axon end of the synapse. This wider bulb surface is implicit of lower tension compared to the shaft of the axom before the bulb at the synapse. It is sort of analogus to oil and water with the smallest bubbles having more tension. As the bubbles get larger the tension or potential with the water lowers. Or the bulb end reflects a lowering of surface tension indicative of this being near a zone where the positive potential drops off.

 

This could also be deduced directly from the firing of the dendrites. Based on this when an axon goes hunting to make a synapse, say on a dendrite, since its little tip is very high in potential, it is going to look for the soft spots on the dendrite which appear to be at the lowest potential. This is reflected by all the right stuff on one spot on the dendrite surface. If it is not the right stuff, the surface potential is too high, such that the axon tip is repelled causing it to continue its search.

[iNow]

Thanks for the extra details and clarifications.

It was truly my pleasure. Thanks for giving me to the motivation to open up some long dormant knowledge.

 

 

The idea of the brain's neuron surfaces being loaded with positive charge, that needs to lower, cuts to the heart of why we need synapses.

I'm confused by this. We have synapses by virtue of the fact that we have neurons. The synapse is the space between neurons. So, saying that the neurons are loaded with charge is the reason we need synapses seems contrary to the much simpler anatomical description.

 

 

This could also be deduced directly from the firing of the dendrites.

Now, I know for a fact I've corrected you on this before, but dendrites are a part of the neuron which receive the signals from other nerve cells. There are two types of dendrites, basilar and apical, the former more common in the body and latter more common in the cortex. They don't "fire," but receive and transmit signal.

 

 

Based on this when an axon goes hunting to make a synapse, say on a dendrite, since its little tip is very high in potential, it is going to look for the soft spots on the dendrite which appear to be at the lowest potential. This is reflected by all the right stuff on one spot on the dendrite surface. If it is not the right stuff, the surface potential is too high, such that the axon tip is repelled causing it to continue its search.

 

We still do not fully understand the entire mechanism responsible for increasing axonal filopodia (axon extrusions into the cytoplasm), but there is EXTENSIVE work indicating that glutamate is responsible for mediating synaptogenesis, or in simpler terms, the growth of new connections between axons and dentrites. The growth of dendritic branches is directly influenced by glutamate, as well as AMPA, NMDA, actin, calcium ions, and glial cells..

 

Considering this information, I'd suggest that your proposal of this process being entirely mitigated by aggregate potential gradients unnecessarily limits the true scope of this body of research and also ignores mountains of existing evidence.

[Revenged]

I think you are missing the point pioneer...

 

All cells within the body have a negative charge - not just neurones...

 

This is because we need to have higher levels of potassium ions inside cells than outside cells... In order to maintin this we need to have a negative charge... That's the basic reason why cells need a negative charge...

 

 

Also, activation of nerves only changes the potential difference at the membrane of the nerve...

 

The concentration of potassium and sodium within the nerve (not at the membrane) is constant...

 

The activation of the nerve has vertually no effect on the overall concentration and potential difference within nerve cells (apart from at the membrane)...

 

The idea of the brain's neuron surfaces being loaded with positive charge, that needs to lower

 

Nerves have there own way of ensuring that the nerves maintain their negative resting potential after a nerve impulse...

 

When a nerve is activated...

 

1) Sodium channels open increasing permability of Na+

(Na+ enters and membrane of nerve becomes positive)

 

2) Potassium channels open increasing permability of K+

(K+ enters and membrane of nerve becomes negative)

 

3) Refractory period

(This is where nerve cannot be activated since the membrane has become too negative)

 

Typically, the activation of nerve takes 1 ms and there is a 1 ms refractory period after the nervous impulse...

 

So the brain's neuronal surfaces are not loaded with positive charge...

 

 

The sodium-potassium pump then pushes the Na ions out of the cell and the K ions are pumped back into the cell, and the original distribution of those ions are restored.

 

The recovery of a neurone from hyperpolarisation to resting potential is passive and is not due to the action of the sodium/potassium pump...

[iNow]

The recovery of a neurone from hyperpolarisation to resting potential is passive and is not due to the action of the sodium/potassium pump...

This last quote to which you responded was mine, and your response is not correct. The repolarization and return to resting potential is exactly the result of the activity of the sodium-potassium pump. Here is a very simple animation provided by the MCB-HHMI Outreach program at Harvard which specifically supports my point (for reference, this particular point is covered on slide #5):

 

http://outreach.mcb.harvard.edu/animations/actionpotential.swf

[Revenged]

This last quote to which you responded was mine, and your response is not correct. The repolarization and return to resting potential is exactly the result of the activity of the sodium-potassium pump. Here is a very simple animation provided by the MCB-HHMI Outreach program at Harvard which specifically supports my point (for reference, this particular point is covered on slide #5):

 

http://outreach.mcb.harvard.edu/animations/actionpotential.swf

 

Course I'm correct... I'll explain a bit...

 

The reason why the membrane goes from hyperpolarisation to resting potential is because of the closure of potassium channels... It occurs passively...

 

http://www.scielo.cl/fbpe/img/bres/v39n3/fig20.gif

 

Look at the graph in the link... You can see that the conductance (movement of ions) of potassium falls...

 

- Closure of potassium channels

- Reduces potassium movement into the cell down the concentration gradient

- Causes the membrane to become less negative

- This causes the membrane potential to change from being hyperpolarised to the resting potential...

 

I was told that this alone explains the change in potential difference... The action of the Na+/K+ pump during an action potential is minimal and the concentration of Na+ and K+ within nerve cells essentially remains the same before and after an action potential as there is basically no difference on the overall concentration of sodium and potassium within the neurone before and after the action potential (only at the membrane of a neurone does the potential difference of the membrane changes)... All activity in an action potential is due to the massive permeability changes in the membrane and the mass opening and closing of Na+ and K+ channels... A lot of people think that the action potential is caused by changes in potassium and sodium ion levels within neurones but this is not the case... it would be physiological impossible to get such dramatic changes of ions in cells within ~1ms (the time an action potential takes)...

 

I think the Na+/K+ pump is only important in maintaining the overall concentration of Na+ and K+ within the cell and this is all... It's main role is ensuring that the resting potential is maintained... but as i said before, the concentration of Na+ and K+ in neurones barely changes before and after an action potential and so the overall effect of Na+/K+ pump is pretty much nothing when compared to the reduction in permability of potassium...

 

Does that make sense?

[iNow]

The action of the Na+/K+ pump during an action potential is minimal and the concentration of Na+ and K+ within nerve cells essentially remains the same before and after an action potential as there is basically no difference on the overall concentration of sodium and potassium within the neurone before and after the action potential (only at the membrane of a neurone does the potential difference of the membrane changes)...

Since this is counter to the information above in my posts, information for which I shared references, would you be so kind as to offer some citations that support your statement (paraphrased) “concentrations of Na and K ions inside the neuron are stable?” Also, to be clear, my reference to the pump was post-action potential.

 

 

All activity in an action potential is due to the massive permeability changes in the membrane and the mass opening and closing of Na+ and K+ channels... A lot of people think that the action potential is caused by changes in potassium and sodium ion levels within neurones but this is not the case...

Didn’t you just contradict yourself? You first said that action potentials are due to opening of Na and K channels (the opening of which changes concentrations of those ions inside and outside of the nerve cell membrane), yet you then went on to say that people who think changes in these levels cause the action potential are wrong.

 

Can you clarify, as you’re not making sense, and I have a feeling that you know what you’re saying but just mistyped it here.

 

 

I think the Na+/K+ pump is only important in maintaining the overall concentration of Na+ and K+ within the cell and this is all... It's main role is ensuring that the resting potential is maintained...

And since the resting potential must be restored after the action potential, the Na/K pump is active during this process.

 

 

Does that make sense?

Well, I follow what you are saying, however, it's not self-consistent and some of it is contrary to existing knowledge. The pump helps restore the resting potential, and I was not arguing for it's responsibility in action potential transmission. For the cell to repolarize though, energy is required, it's not passive (as supported in the above posts I've made with multiple citations), and the non-passivitity is further reinforced by the fact that the Na/K pump consumes ATP during repolarization.

[Revenged]

Since this is counter to the information above in my posts, information for which I shared references, would you be so kind as to offer some citations that support your statement (paraphrased) “concentrations of Na and K ions inside the neuron are stable?” Also, to be clear, my reference to the pump was post-action potential.

 

I just checked and you were right about the Na+-K+ pump... I apologise ... Just ignore what I said before...

 

Didn’t you just contradict yourself? You first said that action potentials are due to opening of Na and K channels (the opening of which changes concentrations of those ions inside and outside of the nerve cell membrane), yet you then went on to say that people who think changes in these levels cause the action potential are wrong.

 

No, you misunderstood... Perhaps I didn't explain clearly enough... I know that there is a change of potential difference... I'm not suggesting that Na+ opening doesn't cause depolarsation or K+ opening doesn't cause repolarisation...

 

What I was trying to say was that action potential is only detectable at the axon membrane... It's only the edge of the membrane that there is a massive change in potential difference... The action potential is a propigation of sodium ions along the axonal membranes... In the middle of an axon I don't think much happens at all and the overall concentration of solutes within a neurone is pretty stable as all the activity only occurs on the surface membranes of the axon and it is over very quickly (~several millisecs)... sorry i can't find any references on this... but i think that the overall change in concentration is very small (~0.01mM???)...

 

I think it's a common misconception is that the entire neurones depolarises and repolarises during an action potential when it reality it only happens at the membrane of the axon...

 

That was all...

[iNow]

I'm not suggesting that Na+ opening doesn't cause depolarsation or K+ opening doesn't cause repolarisation...

I suppose this is good, since that's not how it works.

 

What I was trying to say was that action potential is only detectable at the axon membrane... It's only the edge of the membrane that there is a massive change in potential difference...

What do you mean "only detectable at the axon membrane?" I ask, because if you are implying that action potential action is limited to the cell membrane, you are mistaken. However, if you are implying that we haven't really been able to measure an action potential without measuring the whole cell (see methods section of this link here for details on the perforated configuration of the patch-clamp technique), then you are basically correct. The bigger point is that, just because our measuring equipment is not sufficient to detect change within the cell does not mean that no change within the cell is occurring.

 

 

The action potential is a propigation of sodium ions along the axonal membranes...

 

Just as I stated in post #2.

[Revenged]

The bigger point is that, just because our measuring equipment is not sufficient to detect change within the cell does not mean that no change within the cell is occurring.

 

Ok, i get you... Cheers

 

I suppose this is good, since that's not how it works.

 

[yasitha2]

I don't think there is anything to with action potentials and the brain function. Of course you need action potentials to send the signals. But the brain function depends on how these action potential are modulated. Visit Sciencetoday.