Oh yes, I enjoy your spin on things neurologic. Some obviously don't, some
obviously can't see past the humorous jibes to appreciate that there is
considerably more than just linguistic fun going on, some obviously have
their heads so far up their arse they can only see they own shitty
"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
> 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
> 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.
> 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
1. Strong prenatal stress can permanently heighten HPA axis sensitivity.
2. Severity of depressive episodes predictive of future likelihood of
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 ...
> And, it is already sufficiently obvious that this kind of conditioning
> causes chronically 'sensitized' (loosely so to speak) state in neurons
> functional specialization is to motivate fear and flight-or fight
>> And, it is likewise clear enough that the masqueing (gating) of, and
> obviously possible rerouting of the firing/signaling response of these
> neurons (as a result of a trauma), makes for a _truly insidious
> though originally environmental) kind of stressor_.
>> Physical and psychological pain from individuals' interactions with
> environmental adversity is in _some_ such life-situations 'imploring of' a
> "selective Hibernation" (IOW repression, or "pain gating") response.
Running away basically.
> This on the whole because such a response is the most adaptive survival
> strategy available.
>> Our "AEVASIVE" (~= neurosis capable) brains have partly evolved as an
> augmentation of states of such 'selective supression of self'.
Interesting given that in severe depression individuals can lose their sense
> Presumably repression is mostly and primarily carried-out by GABAergic
> feedback circuits -- the less rapidly activated and much more inertly
> endoopiates (endorphins, enkephalins dynorphins, etcetera) being at the
> 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.
> _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,
> 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
> 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.
> It is not often clearly recognized, that mankind is to a very important
> extent psychobehaviourally co-motivated by (primarily glutaminergic)
> from/by neurons that insidiously as if "reverberate" (or "remember") the
> individual's past environmental stressors (stressors of slowly traumatic
> 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,
hence my previous comments re multiple processes with a final common pathway
vis a vis 5ht depletion.