Auditory Impulse Travel and Distance

Steve Lehar slehar at park.bu.edu
Tue Jun 18 07:45:20 EST 1991

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.
(O)((O))(((               slehar at park.bu.edu               )))((O))(O)
(O)((O))(((    Steve Lehar Boston University Boston MA     )))((O))(O)
(O)((O))(((    (617) 424-7035 (H)   (617) 353-6741 (W)     )))((O))(O)

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