Reference no: EM131271686

Myelin and Membrane Potentials

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There are lots of kinds of neurons and each one has a membrane that is important for its function. Some axon membranes have a myelin sheath and all cell membranes have a membrane potential. Is it clear how the myelin works in relation to the membrane? Is it clear what a potential is? Please respond to one question about potentials and to one question about myelin.

Background on potentials. In videos 4 and 5 (Week 2 Course Content) you will need to be comfortable with ions. You can think of an ion as an atom with too many electrons or too few. Ions carry an electrical charge. Normally there are more negatively-charged ions inside the neuron than outside. This creates the resting potential. Whereas the resting potential is a persisting "default" condition, the action potential is momentary. It's a travelling collapse and restoration of the resting membrane potential, when so many sodium ions enter the neuron that its inner negativity collapses. (It looks like fun.)

For more on the action potential, try this one or that one or the one over there. You can see how the resting potential and the action potential compare at this site, a physiology chapter. Back up to p. 45 to start chapter 2.

In both kinds of potential, ion movements, or currents, are necessary to sustain the potential. One "potential" source of confusion is the fact is that the action potential is not just a voltage (which is another name for a potential) with ion movements. The whole shebang moves along the axon like a riverboat calliope on the Mississippi, taking in sodium and expelling potassium. (If you prefer a duller picture, the ions move up down through the membrane like pistons, while the action potential moves forward like the car. Want to guess what prevents the action potential from moving in reverse? Dr. Suzuki covers that in video 4 as the refractory period.)

In many of our axons the action potential leaps along the axon in a pattern called saltatory conduction. It jumps from one node of Ranvier to the next, much faster than an unmyelinated axon could support. Though we have many myelinated axons, myelin is pretty rare in the nerves of invertebrates. All of the white matter in our brains gets its appearance from myelin, which follows below.

Questions about Potentials (Answer one.)

• In a resting potential, sodium ions are always available in the extracellular fluid but they rarely pass into the neuron. Is it clear why?

• In an action potential, sodium ions suddenly gain access to the inside of a neuron. Can you explain why in your own words?

• In an epsp, sodium ions sometimes get inside a neuron, while at other times they cannot get in. In your own words, what controls the timing of the sodium currents-whether sodium can get in or not?

Myelin. In video 3 you find that myelin allows saltatory conduction of the action potential. Why does an impulse that leaps from node (of Ranvier) to node travel faster? You can see an analogy here that sort of explains why. The speed of an action potential increases with myelination and with the radial size of the axon.

Oligodendrocyte glial cells make myelin when an extension of an "oligo" wraps around part of an axon many times. Its own cytoplasm is squeezed out, leaving only the fatty membrane layers to be compressed further with more wrappings. Glia do more than anyone supposed just a few years ago.

There's some evidence that neuronal activity--action potentials--is what attracts oligodendrocytes to start forming myelin around the active axon.

Loss of myelin, called demyelination, can have devastating effects in diseases such as multiple sclerosis. You can find a good account of demyelination here, and of inflammation (and Alzheimer's disease) there.

Questions about Myelin (Answer one.)

• Why isn't the whole length of the axon covered from beginning to end with myelin?
• Would you expect more myelin around an axon to work better than less myelin? Why?
• Neurons are surrounded by extracellular fluid. Why don't axons with thicker myelin sheaths sink to the bottom of the brain?