Myelination and Regeneration of Neurons
Objective 7
Discuss how the myelination of axons changes their electrical properties.
The nerve cell axon, and many dendrites, are long tubes that are negatively charged inside. If there are no or few ion channels, it acts like a wire, with passive spread of current in the form of positively-charged K+ ions spreading away from the site of depolarization. The positively-charged sodium ions enter through the voltage-gated Na+ channels and repel K+ ions in the region of the voltage-gated channel. As the K+ ions are repelled away from the entering Na+, they form a current.
Because of the presence of leakage channels, this current spread eventually decrements to a point of near-nothingness. This was illustrated in the previous chapter.
In some axons and dendrites, this is a feature of how they work. For example, in dendrites, the decrement in electrical energy is used to transform information flow in a process called temporal and spatial summation.
If the neuron needs to send information over a long distance, however, then it becomes a problem. Either the axon has to be completely coated with voltage-gated sodium and potassium channels, or we can space them out but stop current loss in between the patches that have no channels. In that case, as seen in the purple line in the graph at right, a sheath of lipid called myelin acts as an insulator to decrease the amount of current loss. Axons that carry a myelin sheath are called myelinated.
In the central nervous system (CNS), myelination is the responsibility of oligodendrocytes. In the peripheral nervous system (PNS), myelination is the responsibility of Schwann cells. At the end of this objective, we’ll see how these different glial cell types are reflected in a difference in the capacity for axon repair after nerve damage.
Axons that are myelinated conduct action potentials faster than unmyelinated axons.
Axons that are larger conduct action potentials faster than smaller axons.
This diagram is longitudinal (lengthwise) cross-section through an axon. To the right and the left are myelin sheaths. In the center is a gap in the myelin sheath called the node of Ranvier.
We saw that the action potential depends on the coordinated action of voltage-gated Na+ channels and voltage-gated K+ channels. That supposes that ions (Na+ and K+) can move through those channels. But ions can’t penetrate the myelin sheath, so no action potentials can be generated in those regions of the myelinated axon. The only movement of ions occurs within the “wire” of the axon through passive spread, as discussed in the previous objective.
So we put all of our voltage-gated Na+ channels and voltage-gated K+ channels at the node of Ranvier. Now between the nodes, where myelin covers the axon, there is rapid passive spread of current. The axon is “tuned” to its length constant so that by the time the passive current spread reaches the next node, there’s just enough potential energy (voltage) lef