Somasimple seems to have some kind of axe to grind against the Hodgkin-Huxley theory of how action potentials are generated from electrochemical gradients and propagated down an axon.
It is in the spirit of science to question things. My take is that so long as nobody kills or harms each other over differences in ideas then I see disagreement as a very very good thing (in fact, it is the horrible necessity of progress). Of course, people DO kill and harm each other over differences in opinion...so *ahem ahem*, in light of that observation, 95% of the time when I encounter someone with a different opinion, my response is to simply keep my ideas to myself. You would be amazed at how many times I have typed out these long posts here on PF only to delete them before posting, because I did not want to risk my ideas provoking a negative response in the person on the other end...
You will not be disappointed. I haven't had a chance to really look at the 5th edition yet, but the 4th did a better job on the cell bio topics than pretty much every other dedicated cell bio text that I have seen.
My understanding (which appears to be similar to your explanation) is that movement of sodium or potassium changes the membrane potential not by adjustments to the concentration, but by movement of charge- that way small numbers of ions have a large effect on the membrane potential. Conversely, calcium movement does operate by concentration, because the intracellular Ca++ concentration is so low.
Chloride is intermediate- as you point out, the concentration gradient is small, so ions can flow either way depending on the details of the membrane potential. Plus, paracellular transport of Cl- is usually invoked to "complete the circuit" and maintain overall charge neutrality. So, just as the rule of thumb is that "water follows sodium", I guess "chloride follows charge".
As for the role of chloride in osmotic processes, I am sure all these ions and their individual concentrations have to be very carefully regulated to ensure proper balance. As far as signal transduction processes go, I don't see osmotic balance as too much of an issue per say, because of the rapid way with which the concentration gradients are manipulated and restored to balance, and the small size of the concentration changes with respect to the cytosol as a whole. Certainly in the case of a defective ion channel (such as in CF) where balance cannot be restored properly and the mistake "piles up" over time, the importance of establishing osmotic balance for these channels becomes readily apparent.
As far as the movement of charge itself being the dominating force (at least for external plasma membrane ion channels) as opposed to concentration, everything I have read lately points to that idea being right on. In my understanding, the 2nd term of that above equation dealing with the impact of charge on the process is THE critical contributor to the functioning of the voltage gated ion channels that appear on the external plasma membrane (intracellular channels such as the calcium channel in the ER lack a strong membrane potential and can be an exception, which I will get to in a minute). This is further reinforced when you consider that chloride is generally NOT kept with a small concentration gradient (yes, one of the many puzzling things about it); in fact, in most cases the concentration gradient is the same for chloride as it is for sodium. For example, in squid axon sodium is 440 mM outside and 50 mM inside whereas chloride is at 560 mM outside and 40-150mM inside. Yet, it is known that at least in neurons, chloride moves against the concentration gradient in its ion channels. My thinking is that the concentration gradients are set up to create, maintain, and tweak the membrane potential while the rapid changes in the membrane potential itself (created by opening or closing channels a bit too long compared with the norm) control the actual movement of ions and initiate the main responses (this is sort of clouded by the fact that sodium has *both* an inward concentration gradient and an inward electrochemical gradient for it that together "push" sodium into the cell when its channel opens, prompting explanations to focus on either one or the other).
Indeed the sensitive membrane potential, and not concentration, now seems to be the main driving force for the proton channels used in the production of ATP, at least for eukaryotes (plants do seem to use the "old pH model" that gets taught in schools which I won't get into here). This became apparent once they found out that the eukaryotic membrane wasn't "hording" protons in a little comparment like it does for intracellular calcium or in plants, but that hydrogen ions were free to diffuse away from the plasma membrane and become diluted throughout the cytosol. It is like dropping a bottle of concentrated hydrochloric acid into the ocean (which I should mention here is something that nobody should do); ten minutes later, if you stick a piece of pH paper into the same spot of oceanwater you will get the pH of the ocean and not the acid. External pH cannot be the driving force in such a situation. Yet, protons are driven through the proton ion channel to make ATP just the same...so the conclusion was reached that it actually was the negative membrane potential (with a small effect in proton concentration differences) that largely seems to pull the protons in. Of course, if you gave that answer in your typical college class on a test you will probably be marked wrong (even if some of the more recent cell bio texts such as "The Cell" by Albert, Johnson, Lewis, etc. do implement this somewhat more modern view).
The steep concentration gradient for calcium can be an exception to this as calcium channels are also used on internal membranes (such as the ER) that do not have the same strong membrane potential as the external plasma membrane does. Thus, two additional things are done so that the concentration term can dominate in the Gibbs for Ca in this instance: 1) Calcium is kept in a small sealed compartment (preventing the "ocean diffusion" idea from above and keeping the Ca concentration in the region of the channel very high), and 2) the concentration of Ca in the cytosol is kept extremely low. Of course, calcium can also function with ion channels on the external plasma membrane, and I suspect that as with Na,K, and Cl channels that in this instance once again the membrane potential become the dominant force over concentration, even for calcium.
These sort of ideas about the electrical potential are out there now, but they do not seem to get the same amount of "press" as the concentration concept because concentration differences DO still contribute and it is simply much more easy to understand than a more full picture that takes into account electrical potentials from Physics (and hence, the poor poor chloride ion channel, which then runs counter to the "easy model" about concentration gradients and ion movement, gets regulated to the "zit" status as the tendency seems to be more about covering it up and hoping it will just go away rather than probing deeper into its function...).
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