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A Theory of Neuropeptides?

k p Collins kpaulc at [----------]earthlink.net
Thu Jan 8 03:42:55 EST 2004


Hi Peter.

"Peter F." <effectivespamblock at ozemail.com.au> wrote in message
news:tjVKb.414$Tl1.9573 at nnrp1.ozemail.com.au...

I assume you're replying to my post. [Please leave the
headers when you reply to my posts.]

> You are not wrong!
>
> It is in *every way* plausible (i.e., not just
> because it has been experimentally evidenced)
> that some *key* type glutaminergic neurons
> ("key" in respect of what I am about to suggest -
> or perhaps rather assert and conclude), *can*
> start to release substance-P at a 'certain' treshold
> of excitatory (at least potentially directly distress,
> or flight, motivating) firing, AND at some still
> higher frequency (or same frequency but longer
> duration?) some opioid type neuromodulator.
> [...]

If you check, you'll find all of this is in what I posted.

And it's all discussed, further, in AoK.

"Pain" is a form of "information overload", and "biological
reward" is a servo-mechanism with respect to attentional
"supersystem configurations".

The amygdala plays a role in both, along with the other
TD E/I-minimization mechanisms that are discussed in
AoK, but the amygdala is expressly involved in nervous
systems' handling of "information overload" [in NDT,
"TD E/I(up, up)", or "acelerating TD E/I"].

In my previous post, I was addressing the full specturm
of "information overload", not the "functional multiplexing"
[AoK, Ap9] involved in "pain" and "reward".

Seeing the Neurochemistry without seeing the globally-
integrated TD E/I-minimization dynamics just doesn't
work, Peter.

Take any of the listed pharmacologically-delineated
partial subsystems that you listed in your post, and treat
it as a 'stand-alone' 'information-processing sys-
tem', and all one comes up with is 'alchemy'.

None of them function in the ways that are described
in your list. Everything that's attributed to them occurs
as functions of =globally-integrated= nervous system
dynamics. The studies that attribute such 'functionality'
to pharmacologically-delineated 'subsystems' 'just'
ignore the global-integration, Falsely attributing this or
that to that or this pharmacologically-delineated
'system'.

These studies would have it that, anywhere one looks
within a nervous system, 'there is' whatever they're
looking for - =because= everything that occurs with-
in nervous systems occurs as a function of globally-
integrated dynamics [so some of it is, literally, every-
where within nervous systems [within the brain]].

But what good does Falsely attributing whole inform-
ation-processing dynamics to pharmacologically-
delineated 'systems' do?

None.

But it does 'push folks away from' understanding the
globally-integrated information-processing dynamics.

[In my prior post, I was replying to the previous post
with specific respect to the hypothesis that peptides
sort of 'store information-overload', and I was asking
the poster to answer the question, "Ihen what?" If the
"information overload" is 'stored in peptide action',
then how is that of value within ensuing nervous system
function? And I proposed a way to begin checking out
the hypothesis.]

So, although I'd rather not suffer the consequences
inherent in doing so, I stand on what I posted :-]

Cheers, Peter.

ken [k. p. collins]









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