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Efferents for raphe nuclei

Peter F fell_spamtrap_in at ozemail.com.au
Sun Mar 23 22:54:02 EST 2003

"John H." <johnh at faraway.xxx> wrote in message
news:Ldkfa.310$OZ6.14963 at nnrp1.ozemail.com.au...
> What I am hoping to do, perhaps vainly trying to
> do, is find out what really causes depression. This serotonin emphasis
> ignores the multiple means by which depression can arise, we are attacking
> the problem from the wrong angle. There has to be a better way.

> I want to know which efferents drive serotonin prodn in the raphe nuclei.
> suspect serotonin depletion is an end consequence of a long chain. The
> common pathway of a number of potential processes.

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;

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".

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

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.

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'.

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.

_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.

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).

In other words, when an individual ends up in a "selective Hibernation
imploring type situation", then it is as if a curse, or better "a CURSES"
(for "Conditioned-in [chronically kept Hibernated, hence] Unconsciously
Remembered Stressor(s) Effecting Symptoms"), is also being "put on" (or,
using Janov's terminology, as if "primal Pain" is created within) that
individual's "Actention (Selection) System".

[Hope you can appreciate the sEPTic humor supplied with this complementary
explanation! :-> ]

Partly thereof I contrived (using _very_ pragmatic prose) the concept
AEVASIVE to stand for something like (e.g.):
'Ambi-advantageously Evolutionarily Victorious' (new version :) Actention
(Selection) System Incorporating Various Endoopiates.


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