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Re: Holloway/Morgan ...the BAH....
Ralph L Holloway (rlh2@columbia.edu)
Wed, 2 Aug 1995 10:50:22 -0400
On 31 Jul 1995, HARRY R. ERWIN wrote:
> Karl Pribram holds that for learning to be possible, there must be
> neuronal death. BTW, the new evidence is that learning occurs at the
> individual dendritic spine, not at the level of the neuron. The
> interesting question is how a neuron can maintain a heterogeneously
> activated collection of synapses/dendritic spines. Jim Olds conjectures it
> has to do with the polyribosomes that have been found associated with the
> spine bases. Since it involves membrane biochemistry, I wouldn't be
> surprised if it turns out to be convoluted.
>
Somewhere there are some calculations regarding how many synaptic
connections there might be on a cortical neuron (visual cortex?) and the
number was somewhere in the order of about 10,000, which if true would
mean that modification at the individual dendritic spine in one neuron
cannot be a neuron-alone phenomena, but must also include some
complicated relationship with the surrounding glia. I am here well out of
my depth, but I recall over the past 30 years several attempts being made
to show glial-glial electrophysiological exchange as well as between
neurons and glia, i.e., that the relationship was more than purely one of
biochemical sustenance. I would be grateful to Harry if he could bring us
up to date on this.
So, with neuron death (i.e. one neuron, say in the visual cortex)
some 10,000 synaptic connections would be lost with what must be
extremely minor functional consequences, underlining the high redundancy
necessary to a holographic model ( I assume Karl still holds to that
model ?). Of course, not all neurons are equal, functionally, and perhaps
the loss of neurons in a gating structure, or one associated with fine
tuning (e.g., striatum, cerebellum) will lead to more "serious"
functional consequences over time. It would be useful to have a refresher
"course" regarding the role of plasticity in dendritic arborization as
seen these days with regard to both selective cell death and neuritic
growth. Our static model of so many neurons-so many connections-and
inevitable loss of neurons through aging surely needs updating.
There was an interesting piece in Tuesday's NY Times Science Section
regarding some MRI work done on people with severe emotion trauma in
which it appears that these episodes can actually damage the nervous
system (e.g., the hippocampus) and reduce the volume
up to 25 % or more, results that seem to imply the action of cortisol in
the brain. Here is another area in which we know just about nothing
regarding individual variation and these processes.
Ralph Holloway
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