Try this one for a <straight> answer:
>The intermittent insulation afforded by the myelin, then, does not allow
>the actual voltage to propagate faster. It performs the same function that
>rubber insulation on copper wires performs. It allows the signal to got a
>little further before it has to be amplified, and so the little ion
>channel switches simply don't have to be turned on and off as often as
>they do in non-myelinated nerves. Ideally, the entire length of the axon
>would be myelinated, but because the resistance/ unit length of the axon
>is so high, it can only be insulated for a short length (maybe a few mm).
Because of phenomena usually termed "cable properties," the electrical signal
degrades as moves along the axon (as does a signal in an uninsulated electrical
wire. Myelin prevents this degradation and speeds transmission at the same
time. The signal starts at the hillock with a spike, then begins degrading as
it travels down the axon. Just when it has just enough potential left to open
enough channels to regenerate the spike (about 1 mm), it comes to a node and is
allowed to do so; then the whole thing starts over. There are all kinds of
formulas for figuring out the exact potentials and how much degradation there
will be at which point, and so on.
The nodes of Ranvier are spaced so that as few spikes as possible are required,
presumably to eliminate that "switching" time. So, a completely myelinated
axon would be unable to conduct as the signal would degenerate and be unable to
renew itself. Conduction is sped up because the potential traveling through
the axon from node to node travels at (or near) the speed of light.
Unmyelinated axons (almost all very short) are slower because they require
continuous renewal of the spike.
If you really want, email me, and I can dig out the facts and formulas from my
old notes.
J. Valla
Behavioral Neuroscience
UT-Austin