Once they get triggered, they can trigger an impulse that can then go down the entire axon, and maybe stimulate other things, maybe in the brain or whatever else this neuron might be connected to. So maybe that stimulus by itself didn't trigger it.
But let's say that there's another stimulus that happens right at the same time, or around the same time. And that happens.
And on its own, that might have caused a similar type of bump right over here. But when you add the two together and they're happening at the same time, their combined bumps are enough to trigger an action potential in the hillock, or a series of action potentials in the hillock.
And so then, you really have, essentially, fired the neuron. So now all sorts of positive charge gets flushed into the neuron. And then purely through electrotonic spread, you will have this electrotonic potential spread down the axon.
Now, this is the interesting part, because we can think a little bit about, what is the best way for an axon to be designed? In general, if you're trying to transfer a current, the ideal thing to do is, the thing that you're transferring the current down should conduct really well. Or you could say it has low resistance. But you want it to be surrounded by an insulator. You want it to be surrounded. So if this was a cross section, you want it to be surrounded by an insulator that has high resistance.
And the reason is because you don't want the potential to leak across your membrane-- high resistance right over here. If you didn't have something high resistance around it, your current would actually go slower. This is true if you're just dealing with electronics. If you just had a bunch of copper wires on one side, and you had some copper wires that were surrounded by a really good insulator, a really good resistor-- for example, plastic or rubber of some kind.
The current is actually going to have less energy loss. It's going to travel faster when it's surrounded by an insulator. So you might say, OK, well gee. The best thing to do would be to surround this entire axon with a good insulator. And for the most part, that is true. It is surrounded by a good insulator. That is what the myelin sheath is. So let's say we want to surround this whole thing with just one big grouping of Schwann's cells, so one big myelin sheath-- which is a good insulator.
It does not conduct current well. So this right over here is just one big myelin sheath right over here. Now, what's the problem with this? Well, if this axon is really long-- and let's say, you know, you're a dinosaur or something. And you're trying to go up your neck, and your neck is 20 feet long. Or even a human being, we're a reasonable size.
And you're going several feet, or even whatever, you want to go a reasonable distance purely with electrotonic spread, your signal, remember, it dissipates. Your signal is going to be really weak right over here. You're going to have a weak signal on the other end. It might not be even strong enough to make anything interesting happen at these terminals, which wouldn't be strong enough to trigger, maybe, other neurons, or whatever else might need to happen at this other end.
So then you say, OK, well then why don't we try to boost the signal? Well, how would you boost the signal? You say, OK. I like having this myelin sheath. But why don't we put gaps in the myelin sheath every so often? And then those gaps would allow the membrane to interface with the outside. And in those areas, we could put some voltage-gated channels that can release action potentials, in order to essentially boost the signal. And that's is exactly what the anatomy of a typical neuron is like.
Figure Efficiency of action potentials for different channel distributions in a 0. The axon with uniformly distributed ion channels is consuming almost 50 times the capacitive minimum current necessary to charge its membrane to AP peak. The least inefficient axon in this figure still is 20 times more expensive than the theoretical minimum.
To check if this inefficiency is specific to the axon, we simulated a simple spherical membrane using the same ion channel densities and physiological data than the axon. We then compare the AP waveform in the spherical compartment and the axon in Figure Note that the recorded APs were elicited by a rather long current injection in the cell. This inefficiency factor is much larger than even notably inefficient axons such as the squid giant axon Hodgkin, ; Vetter et al.
A Simulated and recorded action potentials and B sodium current waveform in a uniform channel density axon Black and in a soma Red. The green curve in A is reproduced from Figure 6 in Baker The recorded AP is elicited by a long period of current injection, and therefore the membrane potential before the AP is not representative of the true resting potential, reported to be mV.
The AP is wider and more metabolically expensive in the axon. Difference of inactivation kinetics between Nav1. Action potentials in this model are much shorter than with the original kinetics for Nav1. These calculations take into account the difference in the amplitudes of APs between the two models. The reactivation of even a small number of channels maintains the membrane potential in a depolarized state longer. This in turn opposes the repolarization of the membrane, leaving more time for the possible opening of other channels.
This positive feedback effect makes APs slightly wider in stochastic simulations, where the possible stochastic opening of channels is taken into account. The discretization of ion channel conductances amplifies this effect, by increasing the minimum conductance.
Since the effect of the opening of each channel is bigger in smaller axons Faisal et al. Our simulations lead to two new findings regarding the metabolic cost of propagating APs in C-fibers.
First, incomplete inactivation of Nav1. This in turn creates very wide APs, which are metabolically very expensive. This value is higher than 4, previously obtained for squid giant axon channels Hodgkin, ; Attwell and Laughlin, , and much higher than the very metabolically efficient channel kinetics Alle et al. However, the latter kinetics are obtained in higher temperatures and these comparisons should only be used as an illustration.
Although incomplete inactivation has been shown to allow fast spiking Carter and Bean, , it is not clear why slow firing fibers such as C-fibers exhibit the same phenomena. Presumably, the very slow firing rates of these high-threshold fibers reduce the impact of metabolic cost of signaling in C-fibers. The very wide APs may have a functional role by ensuring a strong post-synaptic response Klein and Kandel, ; Augustine, , and thus prioritize APs carried by C-fibers.
Another explanation may be that incomplete deactivation plays a role in ensuring transmission of APs in noise-prone thin fibers. It is possible that these channels allow for lower Nav1. The role of the Nav1. More detailed simulations are needed to test this hypothesis. We also find that the cost of propagating APs in axons is significantly higher than that of an AP in a spherical membrane compartment.
In our simulations, the cost of propagating action potentials in axons is roughly three times the cost estimated at the soma. The higher cost is associated with wider APs in the axon than in the soma.
This is in stark contrast with myelinated axons, where the myelin sheath lowers the capacitance and leak conductance of the membrane. As a result, nodes of Ranvier can be placed much further apart.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Akopian, A. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Alle, H. Energy-efficient action potentials in hippocampal mossy fibers. Science , — Attwell, D.
An energy budget for signaling in the grey matter of the brain. Blood Flow Metab. Augustine, G. How does calcium trigger neurotransmitter release?
Baker, M. Bakiri, Y. Morphological and electrical properties of oligodendrocytes in the white matter of the corpus callosum and cerebellum. Black, J. Freeze-fracture ultrastructure of rat C. Expression of Nav1. Pain Sodium channel Nav1. Brain Res. Campero, M. Partial reversal of conduction slowing during repetitive stimulation of single sympathetic efferents in human skin.
Acta Physiol. Carter, B. Sodium entry during action potentials of mammalian neurons: incomplete inactivation and reduced metabolic efficiency in fast-spiking neurons. Neuron 64, — Coskun, U. Membrane rafting: from apical sorting to phase segregation. FEBS Lett.
Dayan, P. Computational Neuroscience. Google Scholar. Faisal, A. Laing and G. Lord Oxford: Oxford University Press , — Stochastic simulations on the reliability of action potential propagation in thin axons.
PLoS Comput. Ion-channel noise places limits on the miniaturization of the brain's wiring. Fitzhugh, R. Computation of impulse initiation and saltatory conduction in a myelinated nerve fiber. Hallermann, S. The myelin sheath is wrapped around an axon in such a fashion, that there are a few gaps in between, these are called the Nodes of Ranvier.
Simply put the impulse jumps from one node to the other node, hence called Saltatory Conduction. Unlike the wiring in outer world, which conducts electricity by the shifting of electrons, within these biological wires the impulses are conducted through hyperpolarizing or depolarizing the membrane. It is slightly tricky, but I will try to explain it as easily I can. Now, there are alot of ion channels on the cell membrane neurilemma of the nerve cells.
These ion channels selectively allow some ions to pass through them, and prevent some of the ions. Now, because of these ion channels, there will be a difference in the net charge either positive or negative on either side of this membrane. If the membrane is preventing certain positively charged ions to come inside the cell, there will be more positive charge outside the cell, or there will be more negative charge inside the cell.
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