The reason why the brain uses neural spiking, and encodes signal
magnitude as spiking frequency is exactly to avoid the degredation
with distance that is experienced by the alternative method of neural
signaling, i.e. the density of ions of a particular charge.
The ions, injected at the site of neural input must diffuse passively
along the neuron, which works ok as long as they don't have to diffuse
too far. When you get one of those neurons with an extremely long
axon however, there may be little or no charge left by the time the
signal gets to the end, so the signal decays with distance.
In a spiking neuron, the diffusion must only travel the distance from
the dendrites to the axon hillock. There, the ions either have enough
charge density to trigger an action potential, or they don't. Once
the action potential is triggered, it is guaranteed to travel the
whole length of the axon, and since each spike is a complete
depolarization of the membrane, there is no distinction between "weak
spikes" and "strong spikes", all spikes are essentially the same.
========[ end of quick answer- beginning of more detail ]=============
Here is a simplistic explaination designed to clarify the dynamics of
neural firing without delving into deep technicalities.
The sodium pump constantly and steadily pumps sodium (+) ions from
inside the cell to outside, until a negative charge is built up inside
the cell relative to the outside. There are a few passive channels
around that allow some of the charge to leak back in at a rate
proportional to the potential difference across the membrane, so that
even though the pumps run continuously, the charge can never build up
too great, but settles at some equilibrium value, where the rate at
which the pumps pump it out is exactly balanced by the rate at which
it flows back in through the passive channels.
Electrically gated channels are also scattered about, and these will
open if the membrane is DE-polarized, i.e. if the potential begins to
break down, the electrically gated channels will make it break down
even more. This creates an unstable situation, because a little local
depolarization near an electrically gated channel, say, from a
chemically gated channel that has just locked on to a transmitter
molecule, will create a larger local depolarization. The electrically
gated channel has a refactory period, so that it can only allow a
little gulp of positive ions back into the cell before it slams shut
again to recover. That gulp of ions diffuses outward, and what
happens next depends critically on the density of electrically gated
channels in the local viscinity. If the next one is too far away,
then the charge will not be strong enough to trigger it, and the
charge diffuses slowly in space and time. If enough of these events
occur however, and close enough in time, then the total positive
charge in the cell will become high enough to trigger even the more
remote channels.
Now the axon hillock is richly endowed with electrically gated
channels in close proximity to each other, so that if a single one of
these were to open, it will set off a cascade of channel openings that
will flood the cell with positive charge in one great pulse. Now
along the axon there are more ion pumps and electrically gated
channels, (positioned at the nodes of Ranvier so that they have access
to the extracellular environment) so that a similar event occurs all
along the axon. You can see that a saturation event like this cannot
occur half-way, either the system fires or it does not.
At the output end of the neuron these spasms of depolarization trigger
the release of pulses of transmitter which cause the injection of
gulps of ions into the postsynaptic cell, thereby automatically
performing a frequency - to - magnitude, or digital - to - analog
conversion of the phasic pulsed signal into an "analog" magnitude of
charge in the postsynaptic cell.
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