gord at homostudy.win-uk.net (G K GRAY) wrote:
>And having done that could you please explain how the pulse
>transmission velocity is *increased* by the myelin wrapping that
>normally appears on certain axons? What physical principles are
>involved and how are they involved in this process?
>With best wishes - Gord
The action potential is faster in myelinated axons because it (i.e.,
the action potential involving movement of ions across the membrane)
occurs only at the nodes. In between nodes the potential created by
the action potential travels through the axon according to the same
principles that govern the flow of electricity in a wire: the voltage
disturbance spreads rapidly in all directions, favoring the path of
least resistance. In the case of the axon, the path of least
resistance is the intracellular fluid inside the axon; some voltage
dissipates out through the membrane and myelin, but enough
depolarizing potential reaches the next node to activate the
voltage-sensitive channels there, causing that node to experience an
action potential.
Briefly, then, between nodes the potential travels at a speed
approaching the speed of light (as does electricity in a wire). At
the node ions move across the membrane, a relatively slow process.
In the unmyelinated axon, exactly the same thing happens, but the
potential cannot travel as far without dissipating out through the
membrane. This limits the distance at which the disturbance can
quickly trigger an action potential. Furthermore, in the absence of
myelin the voltage-sensitive sodium and potassium channels along the
axon are _all_ exposed to the extracellular fluid, so every region of
the axon generates an action potential. This results in a greater
influx of sodium in the unmyelinated axon compared to the myelinated
axon, and therefore more work for the sodium-potassium pump.
Hope this helps,
Jeff Wilson wilsonj at smtplink.ipfw.indiana.edu
visit FUN's home page: http://cvax.ipfw.indiana.edu/~wilsonj/fun.htm