What follows are ideas I have along with established concepts.
Excitable Cells
A cell is a compartment that separates the environment within the cell from the environment outside of the cell. This is due to the cell membrane, which consists of a phospholipid bilayer and proteins (Sperelakis, 220). A cell membrane is selectively permeable, which means that it only allows some substances to cross it (Hickman, 45). Water, which is the most abundant substance in an organism and is the, “solvent for all living matter,” is allowed to freely cross a cell membrane (Silverthorn, 132; Hickman, 20, 46). This is called osmosis. Water diffuses across a cell membrane in order to make the overall concentration of solutes inside a cell equal to the overall concentration of solutes outside of the cell (Hickman, 46). This is called osmotic equilibrium (Silverthorn, 132). Solute particles have to be charged or polar in order to be able to interact with the polar water molecules.
Ions are very abundant in an organism. They tend to enter an organism as components of neutral molecules which then dissociate due to the influence of water. So, an organism overall is electrically neutral (Silverthorn, 130; Sperelakis, 11). Ions can only cross a cell membrane through membrane transporter proteins and vesicles (Hickman, 49). Membrane transporter proteins let some ion types through and exclude others (Hickman, 47). Potassium cations are the most abundant ion type inside a cell, and sodium cations are the most abundant ion type outside of a cell (Sperelakis, 222). The next most abundant ion type inside of a cell are protein anions, and the next most abundant ion type outside of a cell are chloride anions (Sperelakis, 11, 222). Chloride anions are the most abundant physiological anion (Hille, 160; Sperelakis, 11). The membrane potential of a cell is a voltage where the overall electrical charge of the inside of the cell is in reference with the overall electrical charge of the outside of the cell. So, the outside of the cell is regarded as 0 mV or ground (Silverthorn, 162, 163). The ions which a cell is most permeable to and which therefore affect membrane potential the most are: sodium cations, potassium cations, calcium cations, and chloride anions (Hille, 3; Sperelakis, 226, 235). These are the main ion types which cause membrane excitability (Hille, 3).
Structurally, there are two types of membrane ion transporters, channel proteins and carrier proteins (Silverthorn, 146, 147; Taiz, 94). Channel proteins are open at both ends simultaneously, whereas carrier proteins involve a change in conformation that causes only one end to ever be open at a time (Hickman, 48; Taiz, 95). Channel proteins transport ions much more rapidly than carrier proteins do (Hille, 372; Taiz, 96). This is because they are simpler and don’t require a time consuming conformational change in order to work (Taiz, 96; Silverthorn, 148, 185). A carrier protein can only transport up to between one thousand and one million ions per second, whereas a channel protein can transport up to tens of millions of ions per second (Silverthorn, 148; Taiz, 95). With most types of carrier proteins, two different ion types pass through simultaneously.
Energetically, there are also two types of membrane ion transporters, those which involve mere diffusion down a chemical (mass) concentration gradient, and those which involve ATP in order to move ions against their mass concentration gradient, called active transport (Sperelakis, 249, 250). All ion channels involve mere diffusion (Taiz, 96). So, only carriers perform active transport (Hickman, 46, 47). There are two main types of active transport, primary and secondary (Sperelakis, 250; Taiz, 96). With primary active transport, the ions are made to go against their mass concentration gradient purely by ATP involvement (Sperelakis, 250). Primary active transporters are called pumps (Sperelakis, 250; Taiz, 96). An example of these are sodium potassium pumps. With secondary active transport, the kinetic energy of one ion type moving down its mass concentration gradient is used to move another ion type against its mass concentration gradient (Sperelakis, 250; Silverthorn, 151). A secondary active transporter simultaneously binds with a specimen of the ion type that does the pumping by moving down its mass concentration gradient and with a specimen of the ion type getting pumped against its mass concentration gradient, and then changes conformation and releases the ions on opposite sides of the cell membrane. Secondary active transport depends on primary active transport because the concentration gradient of the ion type that pumps the other ion type against its concentration gradient through secondary active transporters is set up by pumps (Sperelakis, 250). Sodium and hydrogen cations are the ion types used which pump other ion types against their mass concentration gradients with secondary active transport (Hille, 3). All major ion types have secondary active transporters. Because of how slow carriers are, and because the membrane ion transporters for active transport in both its forms are all carriers, carriers mainly only set up conditions for membrane excitability rather than cause it.
The two types of channel proteins are gated channels and leak channels (Hickman, 45; Silverthorn, 147). Gated channels are usually closed, which allows for the regulation of a particular ion type through them, and leak channels are usually open, leaving movement of a particular ion type through them mostly unregulated (Silverthorn, 147, 148). All membrane ion transporters only let certain ion types through, but gated channels only let the ions which they’re selective for through under certain conditions. So, they’re even more selectively permeable. Two types of gated channels are chemically gated channels and voltage gated channels (Hickman, 45, 46; Silverthorn, 148). A chemically gated channel activates or deactivates when a molecular ligand such as acetylcholine binds to it (Hickman, 46). A voltage gated channel activates or deactivates by changes in membrane potential (voltage) (Hickman, 46). This is due to the fact that the gates are charged amino acids (Hille, 57; Sperelakis, 35, 429; Silverthorn, 250). The gates get pulled or pushed open or closed based on the charges of the surrounding environment. They only activate after a threshold membrane potential voltage has been reached (Sperelakis, 420). The selectiveness of gated channels and leak channels for a particular ion type is due to the pore diameter and the charge of the amino acids in the pore (Silverthorn, 146; Hickman, 45; Taiz, 95). Cation selective ion channels have negatively charged amino acids lining the pore, and anion selective ion channels have positively charged amino acids lining the pore.
All cells have leak channels, and most cells have gated channels (Hille, 5, 699, 705, 706; Sperelakis, 485; Silverthorn, 161, 163; Taiz, 93). There are only leak channels for some ion types. If there were leak channels for all of the involved ions, then every ion type would simply diffuse down its concentration gradient until they were each equally distributed on both sides of the cell membrane (Silverthorn, 163; Taiz, 90). This would be the case if it weren’t for the presence of the pumps, that is, which will be addressed later. What happens is that when an ion type has leak channels, then it will diffuse down its chemical (mass) gradient through its leak channels until it’s stopped by the electrical disequilibrium created by the impermeability of other ion types. For example, potassium leaks out of a cell where it’s more concentrated, down its chemical concentration gradient. As this happens, it leaves behind an increasingly negative charge inside the cell due to the presence inside the cell of protein and phosphate anions, which are the main intracellular anions, and which can’t leave because there’s no outlet for them (Silverthorn, 160, 163, 164). Eventually, the pull of this intracellular negative charge causes the potassium ions to stop leaving the cell in a net manner (Sperelakis, 249; Silverthorn, 165). That is, potassium ions travel back and forth across the cell membrane at the same rate. So, potassium is in an equilibrium state, where the chemical and electrical components of the ion type reach a stalemate.
Although the chemical component of an ion type is only referring to the mass distribution of the ion type on both sides of the cell membrane, the electrical component of the ion type involves all of the other ion types inside and outside the cell because they are charged particles. When each of the ion types that has leak channels is in an equilibrium state between its electrical and chemical components, that is, is in its equilibrium potential, then the membrane potential of the cell is called its resting membrane potential. Potassium and sodium cations are what mainly determine resting potential (Sperelakis, 235). However, there are far more leak channels for potassium than for sodium. This causes a cell to be up to 40 times more permeable to potassium through leak channels than to sodium (Silverthorn, 165, 248; Sperelakis, 232, 230). So, potassium contributes far more to the resting potential than sodium does. This causes the inside of the cell to be slightly more negative than the outside of it (Silverthorn, 130). That is, there’s excess negative charge inside the cell and excess positive charge outside of it. All of the excess charge is located directly up against the cell membrane because electrical diffusion requires that opposite charges remain associated with each other (Taiz, 90; Sperelakis, 228). The interior of both the cell and the interstitial fluid are electrically neutral (Taiz, 90). The only thing that sodium can do is to slightly dig down these excess charge concentrations. So, when it leaks, it doesn’t create excess charge. It merely diminishes the excess charge created by potassium. When sodium leaks into a cell, it diminishes the excess negative charge inside the cell by its positive charge, and it diminishes the excess positive charge outside the cell since it represents positive charge leaving that compartment. All cells have a resting potential, and in all cells the resting potential is mainly due to potassium (Hille, 5, 722; Silverthorn, 163; Sperelakis, 487; Taiz, 91, 92, 107).
It’s actually sodium potassium pumps which establish the entire resting potential of a cell. This is because the leak channels will simply cause the ion types they’re for to leak until they’re each equally distributed on both sides of the cell membrane if not for the involvement of the pumps. When potassium leaks out of a cell, because sodium leaks into the cell, the potassium will never reach a stalemate between its electrical and mass components since the excess negative charge that it leaves behind in the cell, the pull of which would eventually cause it to no longer be able to leak out in a net manner, gets continually diminished by the sodium leaking into the cell. Also, the excess positive charge that the leaking potassium causes outside the cell, the repulsions of which would eventually keep any more potassium from leaking out, gets continually diminished by the sodium leaving. Additionally, when chloride leaks into the cell following after the positive charge of the sodium, then this causes sodium to leak into the cell even more since it diminishes the effect of sodium reducing the excess negative charge inside the cell and the excess positive charge outside the cell by recreating that excess charge. Although sodium and potassium cause each other to leak and perpetuate each other leaking and chloride and sodium do this with each other, chloride and potassium hinder each other in leaking since, for example, when chloride leaks into the cell, it increases the excess negative charge inside the cell and the excess positive charge outside the cell, both of which hinder potassium in leaking.
However, sodium potassium pumps return sodium and potassium cations back to their original compartments where for every two potassium cations returned, three sodium cations are returned. So, they leave behind more potassium than sodium. They’re slower in putting potassium ions back. The net effect is that each time a sodium potassium pump does a transfer, it moves one cation or positive charge out of the cell, because sodium and potassium both have the same valence or charge of 1+. This maintains there being excess negative charge inside the cell and excess positive charge outside of it, the resting potential gradient dipole (Taiz, 96; Sperelakis, 222, 232, 235; Hickman, 48). Although there aren’t pumps for chloride, the forcing of the characteristic mass concentration gradients for sodium and potassium by the sodium potassium pumps also forces chloride to have its characteristic concentration gradient of mainly being located outside of a cell. So, sodium potassium pumps have to continually work to maintain the correct concentrations. This is called a steady state as opposed to a stationary stalemate. However, sodium potassium pumps aren’t fast enough to handle or deal with ion types diffusing through gated channels since too many gated channels open simultaneously. The situation of sodium potassium pumps being mainly what maintains a cell’s resting potential gradient dipole instead of leak channels is supported by the fact that sodium potassium pumps are found in all animal cells including nonexcitable ones. Because potassium and chloride hinder each other in leaking but both increase the leaking rate of sodium, then the ability of sodium potassium pumps to singlehandedly maintain a cell’s resting potential is due to their ability to outpace the leaking rate of sodium even though it’s augmented by potassium and chloride leaking.
Gated channels allow for changes in membrane potential where they’re the prime movers, and therefore they allow for membrane excitability (Hille, 3, 4, 699, 700). They do this by only allowing the ion type that they’re selective for in each case to be permeable under certain conditions. With chloride, which only has leak channels, although when it leaks it does change the membrane potential, it only does this in response to ion movement across the membrane of sodium and potassium. It’s not the prime mover. However, due to its abundance, it’s still significantly involved with membrane excitability. The different types of membrane potential changes are: depolarizations, repolarizations, and hyperpolarizations. The word depolarize means to undo polarity (Silverthorn, 166). The word repolarize means to bring back polarity. The word hyperpolarize means to make more polar. Each of these is referring to the polarity of the cell resting potential.
With voltage gated channels, permeability only starts after the voltage activation threshold for the voltage gated channel type has been reached, and permeability ends after the deactivation voltage threshold is reached (Sperelakis, 430, 431; Silverthorn, 256, 257). With voltage gated channels, permeability ends due to the channels closing, not due to the ion type reaching equilibrium or a stalemate between its chemical and electrical components, as with leak channels. With acetylcholine receptors, permeability only starts after acetylcholine ligands bind to the receptor, and permeability ends when the enzyme acetylcholinesterase degrades the ligands. An acetylcholine receptor deactivates before each of the ion types which it’s permeable to, sodium and potassium, has reached equilibrium between its chemical and electrical components. If it weren’t for this deactivation, then sodium and potassium would each continue to diffuse down its concentration gradient until there was an equal amount of each on both sides of the cell membrane. This is because they cause each other to diffuse through the acetylcholine receptor by continually changing the membrane potential. The sodium causes the inside of the cell to be more positively charged and the outside of the cell to be more negatively charged. The increasing positive charge inside the cell repels potassium cations inside the cell, and the increasing negative charge outside the cell attracts potassium cations inside the cell. Although when potassium cations leave the cell, they cause the inside of the cell to become more negative and the outside of the cell to become more positive which would eventually stop any more potassium from leaving the cell in a net manner if this was the only factor involved, this is counteracted by the sodium cations entering the cell which restores positive charge inside the cell and negative charge outside the cell. This prevents potassium from ever reaching equilibrium between its chemical and electrical components. Also, potassium affects sodium in the same way. Because there are so many more potassium and sodium gated channels than leak channels, the sodium potassium pumps aren’t able to outdo or outpace the gated channels like they’re able to do with the leak channels. So, a main characteristic of gated channels is that they deactivate before each of the ion types they’re permeable for has reached its equilibrium potential.
With three of the four ion types which a cell is most permeable to, those being: sodium, potassium, and calcium cations; their permeability is mainly due to gated channels. With potassium, although permeability is heavily due to leak channels, it has far greater permeability from voltage gated channels due to the fact that during repolarization it brings the cell’s membrane potential from a positive value to a negative value that’s lower than the resting potential, which is created by potassium leak channels (Hickman, 714, 715; Sperelakis, 428, 438). With sodium, permeability is almost entirely due to voltage gated channels and to acetylcholine receptors, which are chemically gated channels. With calcium, permeability is mainly due to voltage gated channels (Sperelakis, 224).
The permeability of a cell membrane to chloride anions, one of the four ion types which cells are most permeable to, is mainly due to leak channels (Hille, 167; Sperelakis, 223, 235, 435). There aren’t pumps for them, unlike with the other three main permeability ion types (Hille, 3). However, in some cell types they are moved by secondary active transport (Hille, 3; Sperelakis, 223). So, chloride anions mainly help maintain the resting potential (Sperelakis, 162, 227). The concentration gradient of chloride anions, which is mainly outside the cell in the interstitial fluid, is held in place by the concentration gradients of sodium and potassium, which themselves are created by the presence and involvement of the sodium and potassium gated channels and the sodium potassium pumps. So, when the gates open thereby allowing potassium and sodium to travel down their concentration gradients, chloride immediately follows suit in order to readjust its equilibrium state.
Membrane excitability is mainly due to sodium and potassium cations, which is indicated by the prevalence of sodium potassium pumps (Sperelakis, 232, 261). In fact, sodium potassium pumps consume as much as between 10–40 % of all of the energy produced by animal cells (Hickman, 48). Also, although calcium cation permeability is mainly due to gated channels, calcium cations are far less abundant than either sodium or potassium (Sperelakis, 222). Sodium and potassium cations are used to create electrical signals called action potentials (Sperelakis, 427, 428). An action potential consists of sequentially activating voltage gated channels (Hickman, 714). Only cells which produce action potentials are considered excitable (Sperelakis, 438). The cell types which produce action potentials are all three types of muscle cells: smooth, cardiac, and skeletal; nerve cells, and some endocrine cells (Sperelakis, 438). With neurons and skeletal muscle cells, which are by far the most abundant of the excitable cells, action potential depolarization is due to sodium. However, with cardiac muscle, calcium cations assist in depolarization, and with smooth muscle cells, the depolarization is actually entirely caused by calcium cations (Sperelakis, 438).
Repolarization is due to voltage gated potassium channels. For example, with a neuron and skeletal muscle action potential, delayed voltage gated potassium channels are used for repolarization (Sperelakis, 35, 438). The voltage gated potassium channels actually start activating long before the sodium depolarization is finished, but they take so long to finish activating that the sodium depolarization is allowed to reach completion before it gets undone by the potassium current (Sperelakis, 434, 435, 438).
With an animal neuron, sodium causes the resting potential gradient dipole to reduce until there’s electrical equilibrium between the inside of the cell and the outside of it, and then it recreates polarity but in reverse (Hickman, 714, 715). Potassium brings back the original polarity or dipole, the resting potential. It does this by first undoing the reverse dipole and passing the point of electrical equilibrium back into the realm of the original polarity. As mentioned previously, potassium actually hyperpolarizes the cell (Hickman, 714, 715; Sperelakis, 428, 438). Because depolarizing sodium ions take the membrane potential from the resting potential to a positive value, but the repolarizing potassium ions take the membrane potential from this positive value to below the resting potential, this means that more potassium is used than sodium. After the voltage gated potassium channels deactivate, the original magnitude of the original dipole, the resting potential, is brought back by sodium and chloride leak channels. The extra amount of negative charge inside the cell more than the resting potential due to the potassium hyperpolarization causes sodium to leak more abundantly into the cell than otherwise. That is, it causes sodium to leak in a net manner. This causes chloride to also leak into the cell in a net manner, going after the positively charged sodium.
There’s a fixed proportional leaking rate relationship between potassium and sodium where potassium leaks a certain extent faster than sodium. This is partly due to the fact that there’s more potassium in an organism than sodium. So, per leak channel, potassium leaks somewhat faster than sodium. However, it’s mainly due to there being much more leak channels for potassium than for sodium. This rate relationship gets disrupted when membrane potential changes occur which aren’t due to it such as the potassium repolarization overshoot. The overshoot tremendously augments the effect of potassium leakage slowing down and sodium leakage speeding up due to the excess charge caused by the potassium leaking. An extra amount of excess positive charge is created outside the cell and an extra amount of excess negative charge in the cell. Potassium leaking slows down in order to as much as possible not make this situation any worse, and sodium leaking speeds up in order to as much as possible alleviate the disequilibrium. This changing of leaking rates merely gets rid of the extra amount of excess charge so that the only amount remaining is that caused by the potassium leakage.
Sodium potassium pumps can only maintain a cell’s resting potential if it’s already established that there’s excess negative charge inside the cell and excess positive charge outside of it and in the correct proportions. This is because they as well as gated channels have no way of adjusting for unwanted membrane potential changes which disrupt the correct proportional relationships. Because leak channels are unrestricted, they’re able to alter their permeability to deal with detrimental membrane potential changes such as a potassium repolarization overshoot. They provide a means of relieving pressure inside the cell, in a sense. With nonexcitable cells, although there’s not the issue of situations like a potassium repolarization overshoot occurring, if somehow an unwanted membrane potential change does occur in the cell, then the leak channels provide a way to relieve pressure in a sense, to get rid of that detrimental membrane potential change.
Repolarization merely resets the electrical component of the electrochemical gradient of the resting potential. The chemical gradient of the resting potential is reset by carrier proteins such as sodium potassium pumps. Because sodium potassium pumps are carriers, they are too slow to help with repolarizations (Sperelakis, 235).
With skeletal muscle, chloride anions heavily contribute to repolarization even though chloride is mostly only permeable through leak channels (Sperelakis, 435). Chloride is kept concentrated mostly outside a cell due to the fact that the main sodium and potassium concentrations are each held where they’re respectively at by gated channels and sodium potassium pumps. So, as the membrane potential gets more positive from depolarization, chloride anions increasingly leak into the cell drawn towards the increasing positive charge inside the cell and repelled by the increasing negative charge outside the cell (Sperelakis, 435). As the membrane potential changes, the equilibrium potential of chloride continually changes. This means that there’s equilibrium between its chemical and electrical components at each point in time, but because the equilibrium state is continually changing, chloride continues to leak into the cell in a net manner. This is different from, for example, sodium flooding into a cell through gated channels, because with this, sodium never reaches its equilibrium potential in the first place. It heads towards it, but it gets stopped short by the gated channels deactivating.
The resting potential of a cell is what allows for depolarizations to be effective like they are (Sperelakis, 436). For example, with a sodium action potential, in addition to the sodium going down its chemical concentration gradient, it’s also attracted to the net negative charge of the inside of the cell and repelled by the net positive charge outside the cell (Silverthorn, 162). If there was electrical equilibrium initially, then although sodium would go down its chemical concentration gradient, it would immediately be leaving behind an excess of negative charge outside the cell that would immediately pull on it. Also, it would immediately create an excess of positive charge inside the cell which would immediately repel it (Hille, 14). The resting potential gives the sodium a significant initial boost by allowing it to both go down its chemical gradient and its electrical gradient. Also, this sets up the same situation for potassium flowing out of the cell for repolarization, because sodium leaves behind an excess of negative charge outside the cell after it reverses the resting potential polarity, which attracts the potassium, and because after the sodium reverses the resting potential polarity, there’s an excess of positive charge inside the cell which helps to push potassium cations out of the cell.
It only takes a tiny fraction of the ions present to significantly change the membrane potential (Hille, 22). For example, only one of every 100,000 potassium ions has to enter or leave a cell in order to cause a full depolarization (Silverthorn, 166, 250, 257; Taiz, 90). So, the chemical concentration gradient of the ion remains almost completely unchanged (Sperelakis, 11, 223; Silverthorn, 166). Because of the tiny amount of ions involved with each depolarization, many depolarizations can occur before the chemical gradient has to be reset.
The combined actions of sodium flooding into a cell in order to depolarize followed by potassium flooding out of the cell in order to repolarize creates a closed electric circuit of positive current (Kramer, 1053). With biological systems, current is positively charged (Silverthorn, 252). This is because with biological systems, sodium, potassium, and calcium cations are the main producers of electricity, and cations are positively charged (Sperelakis, 35).
One of the most important ion types associated with excitation is calcium, although it’s only found in very small amounts (Hille, 3, 98). It’s mainly located outside of a cell (Sperelakis, 11). Calcium is the last step in every excitation of a general excitable cell (Hille, 4, 5). With most excitable cells, sodium and potassium electricity is used to make signals to perform some nonelectrical task such as neurotransmitter secretion with neurons or myofibril contraction with muscle cells. The nonelectrical task is always initiated by the opening of voltage gated calcium channels which affects the intracellular calcium concentration, and the intracellular calcium supply triggers the nonelectrical response.
The electrical aspect of an electrochemical gradient doesn’t regard ion identity or species. For example, it doesn’t care whether excess positive charge is created by sodium cations or potassium cations, or both. All that matters to it is that the magnitude of the excess charge be maintained. So, if, for example, a potassium cation is contributing to this excess charge, the magnitude of the excess charge can be maintained if a sodium cation takes the place of the potassium cation, because both have the same valence of 1+. Also, the magnitude of the charge can be maintained if one calcium cation takes the place of two potassium cations, for example, because a calcium cation has a valence of 2+. Because on either side of a cell membrane all of the ion types are equally mixed together, there’s continually the situation of ions of the same charge but different identities or species replacing each other in a mass of excess charge as they randomly diffuse around.
Because the electrical and chemical components are independent of each other as explained, when, for example, sodium floods into a cell as part of an action potential, the diffusion of the excess positive charge is much more rapid than the diffusion of the sodium itself because the diffusion of the excess positive charge doesn’t require the involvement of the sodium itself as it propagates since there are cations of other ion types involved. Also, with the excess negative charge that gets left behind in the interstitial fluid, its diffusion through the interstitial fluid is much more rapid than the diffusion of the anions themselves for the same reason.
An ion type will spontaneously move down its chemical concentration gradient even though osmotic equilibrium is already established and even if there’s electrical equilibrium between the two sides of the membrane, thereby causing water molecules to follow in order to reestablish osmotic equilibrium. An example of this is the initial leaking of potassium out of a cell. This is evidenced by the fact that pumps have to be used to return the ions. Also, when ions are pumped against their concentration gradient, water follows in the same way.
The reason that an ion type will diffuse down its mass concentration gradient even though this results in electrical disequilibrium partly has to do with the size of the ions in association with their charge. When a larger ion has the same amount of charge as a smaller one as with a potassium cation compared with a sodium cation, each of which is missing one electron, then the charge has to be distributed over a broader surface area since the larger ion has a larger circumference. Because the charge has to be spread over more territory, then it’s more dilute (Brown, William, 339). This affects its interactions with other ions, both like and opposite charges. Even though there’s electrical neutrality in the interior of both a cell and the interstitial fluid, the interactions between the ions in the extracellular compartment where sodium is predominately located are different than the interactions between the ions in a cell’s cytoplasm where potassium is predominately located. This has to do with how a charge gets surrounded by opposite charges in order to create electrical neutrality. It has to do with how charges fit around an opposite charge. When all that the ions in a compartment have is each other, then they have to make do. However, when the ions in a different compartment become available such as when the gates of gated channels open, then ions in one compartment may find more compatible opposite charges in the other compartment due to geometric considerations which allow for a more ideal arrangement. This is another way of saying that the different ion types or species seek to be uniformly mixed together.
However, a bigger factor for why an ion type goes down its chemical gradient has to do with its interactions with water molecules. Because water molecules are so much the majority of the matter and mass in solution, then they push ions around, shuffle and jostle them around, and dictate their movements. Water molecules’ bonding interactions with each other are primarily in a parallel and perpendicular manner. That is, the matrix or network of water molecules primarily consists of parallel and perpendicular bond arrangements (Berg, 9). This is indicated by the lattice that water molecules form with each other in ice. Ice represents the natural bonding state that water molecules want to have with each other. Water is liquid when thermal agitations prevent the water molecules from being able to have the bonding arrangement with each other that they want. In liquid water, when water molecules bond with each other, heat causes the bonds to break thereby forcing the water molecules to have to make new bonds with each other, and this process just keeps repeating itself. However, their natural inclination remains to form a matrix of roughly parallel and perpendicular bonds with each other, and they continually struggle to do this. Water molecules bond with ions in hydration spheres in a radial manner. Because this disrupts the arrangement that water molecules want to have with each other, then, for example, salt water, where salt consists of ions, resists freezing more than freshwater does.
With an ion channel for a particular ion type, the pore diameter mimics the distance of the hydration sphere’s innermost layer of water molecules from the ion. Because the charges lining the interior of the channel pore are arranged along the length of the pore in a linear manner, instead of a radial one, then this more conforms with the natural arrangement of water molecules with each other. So, the innermost layer of the hydration sphere of an ion that the channel is for relieves strain by opening up and docking with the channel pore. By doing this, it doesn’t have to resist or seek to withstand as much the continual insistence of the surrounding aqueous environment that it adopt a less radial structure.
The bonds in a hydration sphere are in the radial direction. For example, with a sodium ion, which is positively charged, the negatively charged oxygen atoms of the water molecules of the innermost layer of the hydration sphere face inwards towards the cation in order to bond with it while the oxygen atoms of the water molecules of the next layer of the hydration sphere face inwards to bond with the positively charged hydrogen atoms of the exterior of the innermost layer. However, the water molecules in a hydration sphere layer don’t bond with each other since their attention is inwards. The entrance of an ion channel opens outwards like a blunderbuss gun. So, when an ion approaches the entrance of an ion channel for it, after the more exterior, and therefore loose, layers of the hydration sphere have been penetrated through by the thermal jostling of the ion, then hydrogen atoms at the exterior of the innermost hydration sphere layer bond with charges along the interior of the outwardly opening channel entrance. This docking somewhat anchors a hydration sphere to a pore entrance. Once anchored like this, the rest of the hydration sphere innermost layer is more inclined to straighten itself out to relieve strain, which it can do with the innermost layer of another hydration sphere for the same ion type by somewhat encompassing it. This creates a multi hydration sphere complex like a net where similar strain, pressure, or tension is felt throughout the complex. A type of capillary action, with more mobile or free water molecules crawling over more anchored or movement restricted ones, occurs that strengthens the complex. The more specimens of that ion type there are on that side of the cell membrane, then the larger this network is. A larger complex experiences more tension or pressure due to all of the ions in it pushing on each other through like charge repulsions. So, diffusion of an ion type down its chemical or mass gradient is due to it going from where there’s more tension or pressure to where there’s less, going from the side of the membrane that has the larger complex to the side with the smaller one, until the tension or pressure is the same on both sides.
What follows is an explanation for how osmosis works. A solute consists of charged particles because only these will associate with the water molecules of an aqueous solution since water molecules are also charged particles. Each ion of a solute in an aqueous solution has a hydration sphere of water molecules around it. Each hydration sphere consists of multiple layers, where the innermost layer is the most bound to the ion, and the outermost layer is the least bound to it. An ion with a stronger electric field has a larger hydration sphere where the innermost layer is more strongly bound to it than is the case for an ion with a weaker electric field. For example, a sodium cation has a stronger electric field than a potassium cation. So, the hydration sphere for a sodium cation is larger than that of a potassium cation, and the innermost layer is more tightly bound to the ion. This is the case even though a sodium cation is smaller than a potassium cation and even though both are each only missing one electron (Atkins, 291). This is because since a sodium atom has fewer protons than a potassium atom, when it loses the same number of electrons as a potassium atom, then this causes it to go further into electrical disequilibrium than a potassium atom since it constitutes a larger percentage of the total amount of the sodium’s electrons than is the case with a potassium atom.
Water fills a cell like in a bag. So, the water molecules pack tightly inside the cell. Osmosis, which is simply diffusion of water, occurs by water going from where it’s more ordered and restricted in movement to where it’s less so. This is based on hydration spheres. With a hydration sphere, the innermost layer is the most ordered and restricted in motion, and the outermost layer is the least so, which means that its water molecules have the most random movements and are therefore the most free. An ion with a stronger electric field causes a larger amount of water to be more ordered and restricted in motion since it has a larger hydration sphere and because the more interior layers of it consist of more bound water molecules (Atkins, 290, 291). When water molecules are more bound, then they’re more fixed in place. This causes water molecules which are more free to grab onto them and crawl over them. Actually, when a water molecule with more random movements grabs onto a water molecule that’s more bound, then it tends to stay where it’s at bonded with the more restricted water molecule. This is somewhat disrupted by the jostling due to thermal agitations and therefore other water molecules bumping into them.
When water molecules are more restricted in motion, then they’re more stationary because they make more long term bonds, and when they have more random movements, then they’re more mobile because they make more short term bonds. This is as with a group of army driver ants which make a bridge with their bodies to allow the rest of the population to cross some barrier. As the bridge is forming, ants will lock themselves in place while other ants crawl over them in order to take up their own stationary positions. This is also as with capillary action which is where water travels up a tube through a combination of adhesion and cohesion. Water molecules adhesively bond with atoms of the interior surface of the tube. After this bonding occurs, the water molecules remain where they’re at and act like rungs on a ladder for other less bound and restricted water molecules to crawl over as they seek to make a fixed or stationary bond with atoms of the tube. The cohesion occurs by water molecules binding with water molecules which themselves are adhesively bonded with tube wall atoms. The more into the interior and the further from the tube wall you go, the less ordered and more random in motion and therefore the less bound and the more mobile the water molecules are. This is as with the innermost layer of a hydration sphere being the most restricted in motion and the most bound to the ion.
Capillary action is simply caused by water trying to establish the same level of restriction in movement throughout its mass. A water molecule that has completely random movements and motions is being continually pulled and pushed on equally to the same extent from all sides by other water molecules as free and unrestricted as it. So, when any of them pulls on it, it pulls back to the same extent and in the same manner resulting in there being no net movement. Therefore, there’s no inclination for it to go in a particular direction in a net manner. However, if it encounters a water molecule that’s more bound, then it gets pulled towards this because the more bound water molecule is more anchored in place. So, when it pulls on the more bound water molecule, the more bound water molecule doesn’t get displaced like with the free water molecules. The more bound water molecule can move the more free one, but not the other way around. This is how osmosis works. The hydration spheres cause a large percentage of the water to have very restricted movements and to be more fixed in place. The hydration spheres cause the mass of water to be like a fixed framework or network anchored in place due to the packed state of water molecules in a cell. The framework is lined with charges, the dipole ends of the water molecules, which pull on water molecules with more random movements in a net manner. Osmotic equilibrium is established when there’s the same level of restriction on the water molecules on both sides of the cell membrane at which point water has no tendency to cross the cell membrane in net manner.
Works Cited:
(1) Sperelakis, Nicholas. ed. Cell Physiology Sourcebook: A Molecular Approach, 3ed. Academic Press, 2001.
(2) Hille, Bertil. Ion Channels of Excitable Membranes, 3ed. Sinauer Associates, Inc., 2001.
(3) Hickman, Cleveland. Integrated Principles of Zoology, 16ed. McGraw Hill , 2014.
(4) Taiz, Lincoln; Zeiger, Eduardo. Plant Physiology, 3e. Sinauer Associates, Inc., 2002.
(5) Silverthorn, Dee. Human Physiology: An Integrated Approach, 6e. Pearson.
(6) Goodenough, Daniel; Paul, David. “Gap Junctions.” Cold Spring Harbor Perspectives in Biology. July, 2009.
(7) Berg, Jeremy M., et al. Biochemistry, 9ed. W. H. Freeman, 2019.