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Sun Apr 10 21:34:35 EST 2005

French,CAS,in English)the first limit of consciousness is its "narrow
What I mean is that the SAC can be compared to a thin ray of light
us say,a huge complex room full of objects inside,that is the vast
space of memory.
Imagine that you enter in a dark Musée du Louvre,full of
beauties,etc,with only a little laser
torchlight which can only illuminate a surface of 1 cm3 at a time!
Within the vast Musée du Louvre you can only examine,at a time,small
fragments of the
Louvre of only  1 cm3...!!!

Even you are inside this palace how can you see(be conscious)the whole
structure of the
Palace with only such a ridicule torchlight?
What you would need are powerful lights illuminating vaster portions
of the space of the
Louvre or,best,illuminate everything at once,like the sunlight,for

So here is the first dilemma of our consciousness:our memory is like
this Musée du Louvre
and vastly bigger but the capabilities of the SAC are similar to this
grotesque torchlight!
Worse:the SAC can make us "see" in the Louvre only within a limited
range of "light
intensity(metabolism)":if the metabolism of the SAC is too small we
are,nearly,in darkness
and blind(serotoninergic threshold)and if the metabolism of the SAC is
too high we cannot
see anything anymore because we get over the illusion threshold and
become "blind" again!
The second dilema is that the SAC is monofocal,that is we have only
one beam of light to
examine the space of the Louvre.Suffice to say that if we had 1000
beams,we would be able
to see 1000cm3 at a time instead of only 1cm3!

Psilocine shows that it is possible to make consciousness a little bit
polyfocal even in our
primitive nervous system.

So the first thing to do in order to increase the "size",the amount of
consciousness,is to
increase the width of the "beam" of the SAC which means that
consciousness has to
become,permanently,not only polyfocal but vastly polyfocal in order to
illuminate sufficient
portions of the imaginary space-time of our memory or our perceptive
Cholinergic neurons seem to play an essential role in the functionning
of the SAC which
seems,basically,not to have much evolved in mammals.
The same can be said with the other neurotransmitter systems which are
part of the SAC.
The purpose of the future neuromorphogeneticians will be to increase
the "scanning" abilities
and performances of the SAC.
In order to do this they will always have to keep in mind the illusion
problem(which,when not properly controlled in our species lead to the
oneiric or
schizophrenic forms of consciousness)and build NEW control mechanisms
to prevent a more
powerful SAC of ever heating memory over the illusion threshold.
Try to imagine,again,the SAC like a very small radar which
is,permanently,scanning the huge
space of memory.In order to increase the performances of such a system
the most
reasonable choice is to increase the size of the radar and its
scanning frequency.
If the SAC could be made so big and powerful that it could "scan" the
whole space of our
memory within a fraction of a second then we would get a huge,enormous
form of
As I said before consciousness is not in the SAC itself but in the
resonances produced by
this system when it "heats" small portions of Memory.
This is the reason why if we non-specifically heat our Memory,but
under the illusion threshold,
we become,at once,more conscious because we get a bigger amount of

The SAC is a spot modulator of memory metabolism

The SAC is,in fact,a spot modulator of memory metabolism but it is so
weak that it
can,only,modulate exceedingly tiny pieces of the Imaginary space-time
of our Memory.
What we call our daily "awareness" is only such a microscopic fragment
of the immense
Continuum of our Memory...
With different molecules it is possible to have access to more stored
information than during
our normal waking state.
For example,haschisch will enhance connectivity and increase the
quantity of the resonances
going on,at a given time,within the fabric of our Memory,making us
slightly more consciouss
than usual.
While the cogitatiogenic,psilocine,will "defocus" the SAC and thus
make us aware of different
things going on in exoreality simultaneously.
Now we can classify haschisch,also,as not only an illusiogenic
molecule but as a resonance
enhancer.This is the reason why haschisch can be useful in
scientific,philosophic or poetic
research because it enhances creativity if one knows how to control
With this in mind it would be interesting to experiment the
combination of haschisch,a
resonance enhancer,with psilocine,a "defocuser".
What is interesting with my concepts,now,is that they give me,all of a
explanations of things I have never been interested in my life,such as
"attention deficit"!
What is attention deficit?
It is the result of an incapacity of the SAC to focus and
hypermetabolise a memory zone for a
long period of time.
As I said,before,the SAC works a bit like a chaotic scanner:when it
perceives environmental
changes it,immediately focuses on these changes.
What makes us basically different,we,as human beings,from more
primitive mammals is the
time interval on which the SAC can stay focused on a memory zone and
"analyse" it by
A cat or a dog cannot focus for a long time:they genetically "suffer
from attention deficit" thus
making their nervous system poorly performant!
Their way of shifting their attention reminds a bit schizophrenics!
Here we are enlightened with a novel
thing:schizophrenics,evidently,have problems with the
functionning of their SAC.
They are,a bit,like cats or dogs suffering from congenital attention
For some reason their SAC cannot stayed focused as well as normal
people so their SAC will
shift from memory zones to memory zones,resulting in poor attention
and confusion.

What seems to control the focusing ability of the SAC is the frontal

As animals have poorly developped frontal cortex their attention span
is small.Dysfunction in
the working of the frontal cortex(like diminished dopaminergic
activity leading to
hypofrontality)of schizophrenics is,clearly,linked with the equivalent
dysfunctioning of their
SAC : hypometabolism of the frontal cortex would lead to SAC
dysfunction if we reason with
the animal example(that is a small frontal cortex leads to erratic SAC
What is nice with this is that we have,all of a sudden,an immediate
explanation of some of the
underlying system dysfunctions of schizophrenia!!!

a.Hypometabolism of the frontal cortex decreases the control of the
b.This decreased control leads to an instability of the focusing of
the SAC.
c.Consequently,the SAC cannot stayed focused for long periods on a
same memory spot.
e.The result is poorness of attention.

What we do not have yet,is why hallucinations are linked with poor
frontal cortex activity?
One reason could be that the SAC would not only roam around from
memory zones to
memory zones(when not controlled properly by the frontal cortex)but
that it would
hypermetabolise indiscriminately these zones thus,logically,leading to
The positive symptoms of schizophrenia would be linked with SAC
metabolic hyperactivity
driven,for example,by dopamine,etc,while the negative symptoms
consequence of poor frontal cortex metabolism linked to
hypodopaminergicity because
dopamine is an ubiquitous metabolic activator.
This justify the combination of a frontal cortex dopamine
activator(amineptine?)with a SAC
dopamine reducer,like haloperidol,risperidone,etc.

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