jdevlin at pollux.usc.edu (Joseph T. Devlin) writes:
> Well, I'm not certain what models you are referencing but I'd be
>interested in hearing more about them.
i'm not sure either... apparently i'll have to take it over to
comp.ai.neural-nets.
> The only related materials I am familiar with show opposite affects.
>For instance, it's well known that in senile dementia neurons have
>_dendritic_ deteriorization and this is well correlated to poorer
>cognitive performance. Buell & Coleman (1979) and Bertoni-Freddari
>et al (1988, 1990) have shown that gradual impairment of connections
>in normal and pathological aging is in part due to morphological
>changes of the synapse. They claimed that as connections were lost
>a "compensatory" mechanism came into play to increase the length of
>terminals so as to attempt to maintain the total synaptic surface area
>in a region.
ahhh, but this isn't what i'm talking about. here we have a chronic
reduction in the ability of neurons to interconnect. what i'm considering
is an acute treatment with an agent that destroys X percentage of
connections, and then the resultant re-growth after that agent is gone...
i also re-read the article i was posted about earlier (i will try to get
around to bringing that down to the computer center and posting something
definite about it) and it references a claim that in vitro studies of
MDMA showed that it has a biphasic effect on 5-HT neurons. stimulating
their growth at lower levels and destroying axons at higher levels...
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