The chemistry/physics of saltatory nerve conduction

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SUMMARY

Saltatory nerve conduction is facilitated by the myelination of nerve fibers, performed by Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. This process involves depolarization at the nodes of Ranvier, where changes in intracellular sodium and potassium concentrations occur without significantly affecting extracellular levels. The action potential propagates efficiently due to the electrical potential changes across the neuron's membrane, minimizing the energy expenditure of the Na+/K+ pump. A unique case is the axon cap of the Mauthner cell, which demonstrates how extracellular ion changes can influence neuronal function.

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  • Understanding of myelination and its role in nerve conduction
  • Knowledge of action potentials and ion concentration gradients
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  • Basic concepts of electrophysiology and neuronal signaling
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Sophrosyne
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TL;DR
Why doesn't the saltatory nerve conduction signal diffuse to other adjacent nerve fibers?
Saltatory nerve conduction occurs because of myelination of nerve fibers. This is done by Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. From what I understand, it happens because depolarization of the membrane at an unmyelinated area of the fiber (node of Ranvier), causes the potassium concentration to increase in the extracellular environment and sodium concentration to decrease, depolarizing the fiber. This chemical concentration gradient is then transmitted across the myelinated area to the next node, so that the message gets relayed faster and more efficiently. The energy intensive Na+/K+ pump doesn't have to actively work to propagate the signal every step of the way along the fiber.

But looking at a place where there is a whole lot of close and dense intermixing of nerve fibers, like the white matter of the brain, it seems like this would be a recipe for disaster. A concentration change by a Na+/K+ pump at one node could potentially cause a discharge of nerve fibers all around it, creating all sorts of mixed messages.

Am I misunderstanding how this works?
 
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Sophrosyne said:
From what I understand, it happens because depolarization of the membrane at an unmyelinated area of the fiber (node of Ranvier), causes the potassium concentration to increase in the extracellular environment and sodium concentration to decrease, depolarizing the fiber.
The potassium concentration in the extracellular environment is not changing. The important changes are in the intracellular sodium and potassium concentrations. The volume of the extracellular environment is much larger than the volume of the intracellular environment so movement of potassium out of the cell and sodium into the cell during an action potential changes only the intracellular concentrations of sodium and potassium wihtout appreciably changing the extracellular concentrations.
 
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Another aspect is that the propagation of the action potential is the change in the electric potential across the neuron's membrane. The voltage change is what causes ion conducting channel proteins at the next node to open.
Like @Ygggdrasil said there is little change detectable change in the extra-cellular ion concentrations (when doing electrophysiology, the extracellular fluids are usually treated as a ground (electrically speaking)).

There is only one special case that I know of where the electrical effects of extracellular ions influence action potentials, the cytologically (cytology = study of cellular structure) unique structure of the axon cap of the Mauthner cell (a big unique neuron in anamniote vertebrates) that is important to their escape response (a rapid turnng away from any of a number of sudden and potentially dangerous stimuli). The axon cap forms an inhibitory electrically based "synapse" at the axon hillock (where action potentials are initiated). This results in the very rapid inhibition of one of the two Mauthner cells if the other one on the opposite side of the brain. This allows the turning escape response to proceed without interference from the other Mauthner cell simultaneously triggering tuning in the opposite direction.

The relevance here is that the axon cap is forms a small sealed off area around the axon hillock where ion concentrations are changed extracellularly and can affect another neuron's function. Go to the axon cap section and the following 3 or 4 sections of this wikipedia article to read about this. There is also a circuit diagram in the link of what's going on in the cytological regions. The cytological structure of the axon cap is unique and not found in other cases (it would be pretty obvious).

This is a very obscure thing (since it seems to be a one off in all of neurobiology). I only know about it since it is found right in the middle of the anatomy that was involved in my thesis project.
 
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Ygggdrasil said:
The potassium concentration in the extracellular environment is not changing. The important changes are in the intracellular sodium and potassium concentrations. The volume of the extracellular environment is much larger than the volume of the intracellular environment so movement of potassium out of the cell and sodium into the cell during an action potential changes only the intracellular concentrations of sodium and potassium wihtout appreciably changing the extracellular concentrations.

Thank you. Makes sense.
 

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