"k p Collins" <kpaulc@[----------]earthlink.net> wrote in message
news:jK8Lb.16101$6B.13829 at newsread1.news.atl.earthlink.net...
> Hi Peter.
>> "Peter F." <effectivespamblock at ozemail.com.au> wrote in message
> news:tjVKb.414$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'.
>I did not address you, but so far I agree with you! :-)
> 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
>> 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?
It is fun and not necessarily (entirely) false. In fact, or at least to me,
the 'filtering/focusing/fixing' functions performed by certain
neuromodulators correspond to contents qualities/levels and intensities of
Consciousness in a *roughly* (or only very approximate - even very vague -
*but fun to recognize*) neuromodulator-specific way.
But you (people) are of course free to disagree. :-)
>> 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',
I, in my post, tried to at least touch on the fact that *they do*; and that
they do by pre and post synaptic "gating" of amygdala originating axons WHEN
these signal alerts about some "selectiv Hibernation imploring type" adverse
aspect of the individuals current, OR some such PAST (no longer
environmentally caused) life-situation.
Adversity detecting amygdala neurons certainly play a significant and
central role but they are not the only actors in need of occasional (or
chronic - whence a SHITS have been stored as CURSES) moderation by
self-regulatory inhibitory feedback.