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Whats Carrying the Current in Neurons?

  1. Oct 4, 2014 #1
    I was wondering what carries the current between two nodes of ranvier (under the myelin sheath) in a neuron. Books and sources say that the impulse jumps between nodes, but I have not found one that tells me how! Is it through the membrane, across microtubules, through the cytoplasm, or something different entirely?
  2. jcsd
  3. Oct 4, 2014 #2


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    The nodes of ranvier let the current travel across the membrane, but where there's no node of ranvier, the myelin sheath increases the resistance across the membrane significantly, which forces more current down the axon. Additionally, it decreases the capacitance of the membrane; for a parallel plate capacitor, the distance between the plates is inversely proportionate to the capacitance, and this is analogous in the membrane, now with a thicker myelin sheath. The reduced capacitance reduces the time constant of charge redistribution, implying faster traveling charges.
  4. Oct 5, 2014 #3
    Ha! I've had the same question, and my conclusion was that they hadn't found out exactly how yet. But the web is increasing its reach, and when I googled my trawl dragged up this:

    "Most science students can tell you that myelination speeds up action potentials as they move down an axon, but how does this work exactly? In my experience, the subject of myelination is not well taught in schools and so in this post I will try to provide a little bit more depth on the subject.

    As most know, myelinated axons cause signals to travel via saltatory conduction. “Saltatory” comes from the Spanish verb “saltar” which means “to jump”. By wrapping around the axon segmentally, myelin leaves only small nodes open along an axon to which signals can “jump”, these nodes are called nodes of Ranvier. The question is now, are these signals really jumping? (hint… nope.)

    Signals travel down an axon in two ways, electrotonic current spread and action potentials. Electrotonic current spread can be thought of as a flow of ions within the cellular fluid, mostly K+ and Na+. When Na+ flow into the axon via an action potential, it displaces other ions within the cytoplasm of the neuron causing them to move away from the location of the Na+ channels. This movement of charge is the basis of electrotonic current and it occurs very very quickly. For anyone who has done a physics class, it’s easy to recognize that particles at a temperature of 298K are moving fast, much faster than an ion channel can displace ions from the interstitial space into the cytosol.

    It is for this reason that action potentials are actually very very slow in comparison to electrotonic current, so in order to increase conduction velocity down an axon we actually want to minimize the amount of time the signal is being transmitted as an action potential. It is exactly this that myelination accomplishes – the nodes of Ranvier are actually locations at which the signal is an action potential, and they are only necessary because electrotonic current decays over both time and distance. Action potentials are a necessary evil in this case. They refresh the signal, but actually slow down the rate of transmission as compared to an all-electrotonic axon.

    Electrotonic current dissipates for two main reasons – loss of ions due to flow out of leak channels and also time. The farther an ion travels within the cytosol the higher the chances of it encountering a counter ion (Cl-), or having its path blocked by a cellular component. It is for these reasons that we need to introduce two variables for the calculation of conduction velocity, λ the length constant and τ the time constant. The length constant is the length over which the signal will decay below 37% of its initial value, and the time constant is the time required for a membrane to charge.

    Conduction velocity is proportionate to the length constant over the time constant. This should be intuitive – signals which can travel electrotonically for a longer distance without decaying will travel faster. Additionally, membranes which require less time to change their charge will facilitate for faster charge movement.

    By wrapping around the axon, myelin reduces the number of leak channels through which the ions can flow. This increases the length constant, the signal can thus travel further as electrotonic current and will therefore travel faster.

    To conclude, myelin accelerates the rate of signal transduction down an axon for a variety of reasons. First, it decreases the number of leak channels along the axon, this causes ions to remain in the axon and allows signals to travel further as electrotonic current before needing to be refreshed as an action potential. The “jumping” referred to in the beginning of this post is actually the action potentials occuring along the axon and represents a renewing of the electrotonic current – they are a necessary evil and actually slow signal transmission. If there were less nodes of Ranvier then signals would actually travel faster (provided they didn’t die down below threshold). There is no actual jumping along the axon, all current is transmitted within the axon itself and is caused by ion flow."

    [ Quoted from Anthony Isaacsons's blog without asking for permission, as it was posted for students of the subject; http://brainyinfo.com/2013/05/13/how-myelination-works/ ; my bold]

    TL;DR: Nodes of Ranvier acts like signal amplifiers along a long optic fiber cable.

    My own confusion was from understanding nerve signal transmission as solely action potentials triggering massive scales of ion channel openings. (There is always a degree of random openings as "noise", due to the stochastic component of chemistry and hence of chemical machines.) But now I know.
    Last edited: Oct 5, 2014
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