Brain clues to attention disorder

k p Collins kpaulc at [----------]
Sun Dec 21 17:57:46 EST 2003

I retract my recent assertion that I've not read anything
posted by you that mad[e] difference [and 'apologize'
for my comment's deliberate 'heat'].

This discussion you've posted is worth the screen-area that it

"Glen M. Sizemore" <gmsizemore2 at> wrote in message
news:582c15c5f1a4da1d5ffa3127f92df7fe at
> Whatever meaning might be given to the term "psychomotor stimulant," it is
> clear that the term is useless for describing the effects, on complex
> behavior in animals, of drugs like cocaine, amphetamine etc. and related
> drugs like methylphenidate (Ritalin). It has been noted for some time
> in laboratory animal operant preparations, such drugs will decrease high
> rates of response maintained by food presentation, while increasing low
> rates of response, in the same subject within the same experimental
> This led to the notion that the particular event maintaining responding,
> i.e., food, water, shock-termination (usually termination of a stimulus
> is perfectly correlated with shock-occurrence in the absence of
> etc. didn't matter in determining the effects of psychomotor stimulants -
> what mattered was the ongoing rate of response under non-drug conditions.
> Although it is now clear that there are a variety of circumstances in
> the so-called "rate-dependent" effects of psychomotor stimulants do not
> (such drugs rarely increase the rate of punished responding, for example),
> it is still a fact that under a variety of circumstances the effects of
> psychomotor stimulants on positively- and negatively-reinforced behavior,
> laboratory animals, is an inverse function of non-drug rate of responding
> (and dose, of course; small doses of the drugs tend to increase low rates
> response while having no effect on higher rates; moderate doses will
> substantial increases in low rates while high-rates will be reduced; high
> doses will, of course, decrease both high and low rates).
> [...]

This's all 'just' topologically-disdributed E/I-minimization
yielding "inversion" with respect to 'localized' drug-induced

It's all 'just' what's been integrated in AoK all along.

The thing I emphasize is that the neural dynamics that are
being 'treated' with drugs are =not= 'abnormal, but are
the 'normal' activation-dependent nervous system reaction
TD E/I(up)-generating environmentally-induced activation.

It's 'just' "inversion" as it's been discussed throughout AoK,
and in particular, Ap4, left uncomprehended.

To others than Sizemore: "But, what the hell? Why bother
doing all that work to actually understand, when we can
just get rich by pushing these drugs? Besides, we like the
way that Society is being maintained in the darkness, Allows
us to go right on getting rich, and keeps the riff-raft from
knowing any different."

K. P. Collins

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