🚀 go-pugleaf

Sorry, I don't read bionet.molbio.aging, so I've set followups back to
sci.bio.  Perhaps I should have set them to bionet.neuroscience?  In
any event:

In article <575@tdatirv.UUCP> sarima@tdatirv.UUCP
     (Stanley Friesen) writes:

>In article <1992Apr27.105750.17252@yang.earlham.edu>
     allens@yang.earlham.edu (Allen Smith) writes:

>|        In other words, the number of synapses (as opposed to brain cells)
>|goes down as one gets older? Then why does "fixed" IQ increase with age?
>|Is this decline simply due to loss of neurons, or what?
>
>No, to loss of synapses.  Long term memory is based on changing the number
>of synaptic connections between particular pairs of neurons.

I'm curious as to where you got this impression.  I think that
neuroscientists will (in general) tell you that the mechanisms of long
term memory storage are pretty much up in the air, but that changes in
synaptic weight are the most likely current candidates.  That is, a
synapse doesn't necessarily form or retract (synaptic weight go from 0
to 1 or vice versa) but rather the synapse becomes more or less
effective (more transmitter per action potential may be released from
the presynaptic cell, the postsynaptic cell may generate a larger
response to the same amount of transmitter etc. or the opposites to
those conditions).

>However, in any given case the number can either go up or down.  New synapses
>form as well as old ones disappearing.

I'd be even *more* interested to hear where you heard this.  Some of
the best work in adult cortical plasticity these days is coming from
the lab of Mike Merzenich at UCSF.  What he finds is that changes in
the periphery (e.g. stimulation of owl monkey fingers by rubbing them
lightly on sandpaper) causes changes like what I described above.
Sometimes cells which did not respond to other cells later do, but the
effect seems to be limited to a region around 3mm from a given
presynaptic cell.  If I recall correctly, this is also the extent of
the dendritic trees, and the conclusion is that the changes in
responsivity arise *only* from changes in synaptic strength, and *not*
from the formation of new synapses.  The changes can be caused to
occur in a matter of minutes, but last for weeks.  Do you know of
evidence of the formation of new synapses in an adult mammalian
central nervous system?

>The main exception to this is that dramatic loss of synapses shortly after
>birth that William mentioned.  There entire axons wither and disappear,
>presumably along with the originating neuron.  

I think that this presumption is entirely incorrect.  Many neurons
die, but in mammals I believe that this sort of cell death occurs almost
exclusively before birth.  The retraction of axons continues for a
considerably longer period (i.e. years).

>This appears to be the final stage in establishing the primary wiring
>diagram of the brain.  It seems that the genetic program can carry the
>wiring only so far without environmental inputs to select the correct
>subset of the avialable wiring.

There are "critical periods" in development, that are linked with
different sorts of rewiring...  In humans, the critical periods of
some effects (e.g. how old can you be before curing strabismus ("lazy
eye") leads to no difference in stereoscopic ability) last well into
the first decade of life.  As I recall, there are different "final
stages" for different sorts of events.  In the example I gave above,
the critical period is probably yoked to the time during which your
eyes are still growing.  Beyond those periods, any "rewiring" must be
of a fundamentally different nature.  I gather that's what you're
getting at?

>Thus I doubt that the conclusion William made really follows.  Even if the
>trend is mainly downward in adulthood, this may just mean that learning
>is progressive.

I'd call this an open question...

>uunet!tdatirv!sarima				(Stanley Friesen)

Mickey Rowe     (rowe@pender.ee.upenn.edu)