IUBio Biosequences .. Software .. Molbio soft .. Network News .. FTP

Efferents for raphe nuclei

Peter F fell_spamtrap_in at ozemail.com.au
Sat Mar 29 22:56:58 EST 2003


"John H." <johnh at faraway.xxx> wrote in message
news:T1Ega.322$B34.12497 at nnrp1.ozemail.com.au...
> "Peter F" <fell_spamtrap_in at ozemail.com.au> wrote in message
> news:yjvfa.122$WJ.4967 at nnrp1.ozemail.com.au...
> > "John H." <johnh at faraway.xxx> wrote in message
> > news:Ldkfa.310$OZ6.14963 at nnrp1.ozemail.com.au...
> >
> >
> > You seem somewhat tentative (IMO needlessly so) in your opposition to
this
> > widespread stupidity of explanatory emphasis and/or refusal to connect
> > together 'positively overwhelmingly obvious' clues to the a very main
> > category of relevant causes -- a "category" which of course include
> anything
> > from slowly to rapidly traumatic experiences;
>
> Bees to honey, if you want to shift someone's perspective then not much
> point barraging them with criticism; granting that can be great fun -
except
> of course for those with their heads so far up that no amount of honey
will
> shift their pov ...
>
> > Ditto (derogation;) for the common blatant failure to gain insight into
> the
> > fact that active repression (gating) is required in the aftermath of
such
> > experiences having been "condition-in".
>
> Only at the clinical level Peter, mucho good research pointing at what
> you're hinting at.

Actually, I have noticed that, lately (and with pleasure).
Am a bit inert in my anger - I admit. :->

I decided a long while ago not to bother providing references for the "dots"
(by me spotted samples of scientifically established principles therories
interpretations and concepts) by which I have endovoured to plot a sparsely
spaced (but nevertheless in my eyes sufficiently clearly resolved)
complementary (but 'effectively philosophy terminating' or rather
encompassing) picture of "things".

(I.e., mainly and centrally, but not only, of "things human".)

I stopped _only partly_ because my pile of jotted-on (mostly at Libraries)
slips in which I kept my collection of specific relevant samples (as if
siphoned-off from a collectively accumulated 'tank') of "Scientifically
Established Principles/Therories/ Interpretations/Concepts type
informational matter" (both philosophically and practically as if
_predigested_ products of Science-as- a-whole) got lost at home in 'a
spring-cleaning fervour';

Also because I am lazy, disorganized, and don't expect anyone but someone
who is science factually, philosophically, and also otherwise sufficiently
predisposed, to appreciate EPT.

> > It is clear _enough_ that traumatic experiences are condition-in not the
> > least into neurons of the amygdala - i.e., of course, in cases where
these
> > regions have already been 'ontogenetically brought on line' at the time
of
> > trauma;
>
> Eg.
> 1. Strong prenatal stress can permanently heighten HPA axis sensitivity.
> 2. Severity of depressive episodes predictive of future likelihood of
> return.
> 3. Hippocampal atrophy via stress may well be driven primarily through
> amygdala persistent activation of the hippocampus, atrophy here strongly
> implicated in depression and post traumatic stress disorder.
> 4. Overly sensitised HPA axis may initiate sustained plasma il6, thereby
> creating positive feedback loop re future stressors.
> 5. Chronic glucocorticoid expression (beyond the MR occupation to
sustained
> GR occupation) atrophies hippo, induces spatial learning deficits (another
> stressor to an already overburdened brain),
> 6. Dopaminergic regulation of pfc is dynamic and labile, v. high momentary
> stresses or chronic stressors appear to deplete\ change this regulation,
> leading to more deficits, leading to more stress ...

Good of you to list some of the specific means!

In general I _partly_ think of it this way:

The environmentally caused (or by "life-situations" conditioned-in) chronic
states of elevated activity/excitability of (most centrally and directly)
fear/pain/distress-motivating RAT type neurons ["hyper activity" => ADHS] in
_de facto_ question [IOW: "trauma type" memories (i.e., usually unconscious
such), primal pain, engrams, or CURSES] is the most commonly ignored
insidious "generator" (or, to be more precise, *a major co-motivator*
behind) of a wide spectrum of normal (from socially accepted to adored)
AEVASIVE preoccupations, as well as abnormal and/or antisocial such (mildly
neurotic to seriously scary and psychopathic) AEVASIVE behavioural
activities. These conditioned-in "core neural states of excitation" are of
course also then a driving "endogenous" cause of chronically occurring
neurochemical "ebbs and floods" (neurochemical and psychobehavioural
imbalances). The durations of these ebbs and floods and their
psychobehavioural and psychosomatic consequences do of course vary depending
on both DNA-inherited, Histone-code inherited, and otherwise "total
life-situational" _differences_ between individuals.

It is possible to think of how we are partly in terms of whether we
(individually, and collectively culture-specifically) have an exhausted
"defense system".

However, I have found it is "better" (am not boasting) to more unifyingly
understand (and explain) how we are from a perspective that brings into view
the 'almost logically inevitable' fact that we evolved by evolutionary
pressures that caused a natural selection of certain (generally classified
and conceptualized, but also thoroughly defined) "ambi-advantageous"
adaptations.

Thereof "AEVASIVE".

<snip>

> > Presumably repression is mostly and primarily carried-out by GABAergic
> > feedback circuits -- the less rapidly activated and much more inertly
> active
> > endoopiates (endorphins, enkephalins dynorphins, etcetera) being at the
> far
> > other end of our available range of such 'trauma tackling' inhibitory
> > neurotransmitters and modulators.
>
> GABA at a general level, I'm more interested in dopaminergic aspects of
> this; with emphasis on D1 - D2 balance.

Apropos dopamine:
Deprivation of needs (a chronic lack of certain satisfying life-situations)
can when combined with AEVASIVE coping mechanisms reroute the primal
(primarily distressing) motivation into whatever 'dopamine craving'
(whatever kind of addictive) preoccupation.
Hence the scope for anything from highly creative preoccupations (focuses of
actention) to (when the dopamine requiring neurochemistry involved is
exhausted to the point of chronic depletion - at best an environmentally
induced deep Hibernation by centrally affected neurons rather than their
ditto caused "programmed cell-death") mental and motor (Parkinson's)
symptoms of 'neural inertia'.


>
> > _Potentially_ pain/distress/flight or fight motivating signals, are of
> > course most primarily glutaminergic in kind.
> > And since, in the internal presence of an abundance or powerful
> > (neurological) pressure of such potentially distress-motivating signals,
> > repression is seldom perfect, and in fact in many cases quite
inadequate,
> it
> > should not be a surprise that the supply and 'active service' of
serotonin
> > (whose phylogenetically original role might plausibly have been to
trigger
> > feeding behaviour whenever an individual's "total situation" offered a
> > corresponding opportunity) might eventually be "set back" (so to speak).
> >
> > An other important effect of repression (given the kind of neurons'
> > signaling that is being neurologically repressed) is the rerouting and
> > motivational reassignment of the glutaminergic signals in question.
> >
> > This "rerouting" occurs (is possible) as a result of neural sprouting
(in
> > combination with suitable anatomical and microanatomical sites of
> proximity
> > where functional connections might be sprouted) and by the fact that
both
> > deprivation and hypotrophic effects in a down-stream direction relative
to
> > sites of suppression can cause an unmasqueing of normally anatomically
> > pre-existing (as if "probabilistically ontogenetically offered";) but
> > normally (or, rather, ideally) out-competed, functional potentials.
>
> No, I suspect "rerouting" arises through changes in neuromodulatory
> functions - Da, 5ht, nore.

I don't see that what I wrote as conflicting with what you say. You are just
looking at the same thing from a different angle.

If you insist that you do, please let me know what you see!
>
>
> > It is not often clearly recognized, that mankind is to a very important
> > extent psychobehaviourally co-motivated by (primarily glutaminergic)
> signals
> > from/by neurons that insidiously as if "reverberate" (or "remember") the
> > individual's past environmental stressors (stressors of slowly traumatic
> as
> > well as rapidly traumatic type).
> >
> > As you might know, I think such stressors _deserve_ an alternative
label -
> > one that reflect that they "stink" (so to speak), and that individuals
who
> > endured them tend to get stuck with this "stench" (as do, in many an
> > important sense, their offspring down the line, and often others as
well).
>
> Stress is a shitty word, to vague and in desperate need of delineation,

Agree!

> hence my previous comments re multiple processes with a final common
pathway
> vis a vis 5ht depletion.

Thanks again!

P





More information about the Neur-sci mailing list

Send comments to us at biosci-help [At] net.bio.net