Path: utzoo!utgpu!jarvis.csri.toronto.edu!mailrus!iuvax!purdue!gatech!prism!sloth!carter
From: carter@sloth.gatech.edu (Carter Bullard)
Newsgroups: comp.ai.neural-nets
Subject: Re: wanted: neurobiology references
Message-ID: <545@hydra.gatech.EDU>
Date: 24 Apr 89 14:58:09 GMT
References: <4486@psuvax1.cs.psu.edu> <17450@cup.portal.com>
Sender: news@prism.gatech.EDU
Reply-To: carter%sloth@gatech.edu (Carter Bullard)
Organization: ICS Department, Georgia Institute of Technology
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In article <17450@cup.portal.com> mmm@cup.portal.com (Mark Robert Thorson) writes:
>I was taught, 10 years ago, that action potentials are believed to originate
>at the axon hillock, which might be considered the transition between the
>axon and the soma (cell body).  See FROM NEURON TO BRAIN by Kuffler
>and Nichols (Sinauer 1976), page 349.
>
>I would expect synaptic weights to be proportional to the axon circumference
>where it joins the cell body, but I have no evidence to support that belief.

well,
   the idea of synaptic weights emerged principally from neuropharmacology.
It attempted to explain such phenomenon as the changes in the way 
neurons responded to GABA (gama amino butyric acid) in the presence of 
valium, the dopaminergic theory of psychosis and why some antipsychotic
drugs (chlorpromazine) seemed to work best during the morning, altered 
responses to visual stimuli, at the cerebellar level, in the presence of 
amphetamine, in cats,  ..... the list goes on.

   the basic idea is that the transfer of information from one neuron
to the next is chemically based.  To summarize, as the nerve action 
potential reaches the "terminal bouton" (that is the collection of 
synapses that represent the "end" of a neuron), the electrical gradient 
changes on the membrane of the presynaptic neuron set off a set of
reactions that result in the release of chemicals, "neurotransmitters",
into the synaptic cleft.  Because the recipient (post synaptic) neuron
has receptors on its outer membrane that respond to the neurotransmitter,
small deformations in the electrical potential of the target neuron occur.
These are called miniature excitatory (or inhibitory) postsynaptic
potentials (MEPPs).  These electrical changes propagate along the membrane, 
similar to ripples on a waters surface.  The axon hillock, which is a 
specialized area on the surface of the cell body of a neuron, can act as a 
capacitor, of sorts, in that it can "summate" the potential changes over 
time.  It is thought that the threshold for excitation originates at the 
axon hillock, but this is not always the case, as the entire membrane of 
the neuron has the ability to start a nerve action potential.  The axon 
hillock is generally responsible for summating MEPPs.  

   But the ability for a MEPP to cause a change at the axon hillock is
dependant on the distance between the loci of the chemical reaction to 
the neurotransmitter and the axon hillock, the strength of the MEPP, and
the properties of the cell membrane that facilitate the propagation of the
MEPP along the membranes surface.  This is determined by many factors, but 
the topology of the neuron is, indeed, important.

  However, the principle contributors to synaptic weight are generally thought
to be biochemically based.  These include such properties as, the amount of 
neurotransmitter that is released from the presynaptic neuron, the number 
of receptors that are available on the postsynaptic neuron, the effectiveness 
of the transmitter to create a MEPP, the duration of the 
neurotransmitter/receptor association, and the effectiveness of the 
postsynaptic membrane to propagate the MEPP.  

  The amount of neurotransmitter released with any given nerve action
potential is not constant with time, as the transmitter pool that is
available for release is limited.  The history of excitation of a neuron
is important, since neurotransmitters can be depleted with repeated excitation.
This is transmitter exhaustion, and is a real phenomenon that can be 
demonstrated experimentally and clinically.  The factors that determine
presynaptic neurotransmitter availabilty are generally described with 4th
or 5th order non-linear differential equations, depending on whether you
consider the variations in diet or not.

  The number of receptors that are available on the postsynaptic neuron,
their effectiveness to respond to chemical stimuli, and the rate of receptor
turnover has been the subject of pharmacological study for over 50 years,
and is rather complicated.  The best models are 3rd and 4th order differential
equations, where the history of excitation is a prominent factor.

  The ability for the postsynaptic nerve membrane to propagate the MEPPs to
the axon hillock is also dependent on the history of excitation.

  Sooooooo, the number of historical dependants on synaptic weight can be
considered to be rather high.  The topology of the nerve is not that variable,
but the biochemical aspects of nerve function are extremely variable.  It is
probably this and a great deal of other factors, such as the role of glial
cells on neuronal functionality, that contribute the greatest to the "weights"
of a particular neuronal event.
  
Carter Bullard
School of Information & Computer Science, Georgia Tech, Atlanta GA 30332
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Internet:	carter@gatech.edu