Efferents for raphe nuclei

KP-PC k.p.collins at worldnet.att.net%remove%
Thu Mar 27 23:45:11 EST 2003


If you want to see some pertinent stuff, get some volunteer cigarette
smokers who'll agree to undergo stadard scanning techniques whild
doing a long-term study of the effects of stopping and starting
smoking.

Shouldn't have too much trouble finding volunteers. Almost everybody
who smokes wants to 'quit', but almost nobody who quits wants to
stay-quit. [Of course, Ethics require anyone who does want to
stay-quit to be allowed to do so. Ask them to come back into the
study if they decide to start smoking again.]

Anyway, there're profound correlations to what seems to be your focus
[below] that occur =dynamically=, including a chemically-mediated
affective-"inversion" - all of which should show up in standard
scanning techniques.

ken

"John H." <johnh at faraway.xxx> wrote in message
news:T1Ega.322$B34.12497 at nnrp1.ozemail.com.au...
| Oh yes, I enjoy your spin on things neurologic. Some obviously
don't, some
| obviously can't see past the humorous jibes to appreciate that
there is
| considerably more than just linguistic fun going on, some obviously
have
| their heads so far up their arse they can only see they own shitty
| perspective.
|
|
|
| "Peter F" <fell_spamtrap_in at ozemail.com.au> wrote in message
| news:yjvfa.122$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.
|
|
| > 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 ...
|
|
| > And, it is already sufficiently obvious that this kind of
conditioning
| > causes chronically 'sensitized' (loosely so to speak) state in
neurons
| whose
| > functional specialization is to motivate fear and flight-or fight
| responses;
| >
| > 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
| (endogenous
| > 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
| of self.
|
|
| > 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.
|
| > _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.
|
|
| > 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,
| hence my previous comments re multiple processes with a final
common pathway
| vis a vis 5ht depletion.
|
|
|
| Regards,
|
|
| John H.
|
|





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