This removal of positive charges from the cell in turn causes the membrane potential to remain briefly before returning to the resting level [4]. Jump to: navigation , search. Personal tools Log in. Namespaces Page Discussion. Views Read View source View history. This page was last modified on 16 November , at 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. State and location dependence of action potential metabolic cost in cortical pyramidal neurons. Hodgkin, A. The optimum density of sodium channels in an unmyelinated nerve.
B Biol. The Schwann cells form this sheath and they help in fast conduction of impulses across the nerve. Myelin is a fatty white substance, made mainly up of cholesterol, acts as an insulation around a wire. 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.
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