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Autonomic Nervous System

kkollins at pop3.concentric.net kkollins at pop3.concentric.net
Thu Oct 22 22:23:53 EST 1998

First, thank you for your thought-filled reply. Using your post as stimulus,
briefly discuss the way I've approached the problem of all neural
including "LTP", and it's integration.

Hemidactylus at my-dejanews.com wrote:

> In article <362D2136.DD2A4A84 at pop3.concentric.net>,
>   kkollins at concentric.net wrote:
> >
> >
> > Sturla Molden wrote:
> >
> > > There is no evidence that LTP is a naturally occuring
> > > phenomenon.
> >
> > Would you care to square this with what I posted in respons
> to Walter, above.
> > The research report I read did clearly state that Ca(2+)
> dynamics above a
> > threshold have "staying power" (my words)... that is, their
> effects continue
> > after the sub-threshold ionic flow has ceased. What, if
> anything but an
> > LTP-like effect, is this?
> >
> There should be a distinction made between facilitation (due possibly to
> residual CA++ (or inositol mediated release from ER stores?)) and varying
> degrees of potentiation, based on the time interval involved. "staying
> is a relative term. Tetany might bring us into the interval known as
> post-tetanic potentiation (PTP). I have a curiosity about whether LTP is
> nothing more than an artificially induced phenomenon with no correlate in
> natural systems. I think critique of LTP is good.

Critique of =everything= is good, and necessary if we are to stay on track

> >
> > > It araises from repeated tetanisation of
> > > specific neural pathways, eg. in the hippocampus. It is
> > > also not a homogenous phenomenon, there are several
> > > sub-types of LTP depending on different receptors
> > > (eg the NMDA receptor, opioid receptors, mGluRs)
> > > and with different durations.
> > >
> > > LTP depend on the same mechanisms that seem to be
> > > involved in memory formation, but there is no evidence
> > > that LTP is the substrate for memory.
> >
> > Yeah, but show me "memory" without the involvement of LTP...
> only way one can
> > is to show me a "corpse" (brain dead).
> >
> I am presently in search of references that critique the use of LTP as a
> model for vertebrate memory processing. Anybody know where I can find some

> good ones? Perhaps LTP is a good model for memory processes, but I would
> for someone here to give a serious critique.

In my view, one must step back a bit, and consider the system as a whole
one can grasp the roles of any mode of neural activation. The easiest way to
this is to work with a constant awareness of the two "fixed" points... the
primary, sensory and motor activations, and of these, begin with motor
activation. When one grasps a pencil and writes, for instance, only that
activation which drives the effectors of the trunk, arm and hand so that a
particular word will be written is "acceptable"... all other activation must
"stripped away", relative to the "acceptable" activation.

In this, one sees that things are vastly-inhibited... a starting point...
activation that underpins any discrete activation of the effectors must be

Next "level" requires the study of the effector geometry. When one does
this, one
finds that some effectors must be activated relatively-more than others, and
the "waveform" of the activation is very-dynamic.

Next thing is that in order for the effectors to be activated in a way that
accomplishes a task within the 3-D external environment, all activation that

occurs must preserve an "awareness" of the external 3-D geometry. I briefly
discussed how this occurs within our nervous systems earlier in another
(the topology of decussation), and all of that serves as powerful constraint
anything else that can be said about anything, anywhere within the nervous

To sum so far, activation states must be minimal, they must preserve a
geometrical correspondence with the external 3-D environment, and because
effectors are asymmetrically-distributed, the activation that's necessary at
effectors will have to reflect that asymmetry while preserving the necessary
geometrical congruence.

I know this doesn't sound like "neuroscience", but it constitutes =precious=

constraining stuff that, literally, permeates the nervous system,
powerfully-delimiting the set of more-detailed things one must consider. So
grappling with it, until it's mastered, greatly facilitates our going
(The Thermodynamics of the external environment does more of the same, but
save that for another discussion.)

So, if one is to say anything about "memory", all of the above stuff =must=
be in
what one says about "memory". Otherwise, one is confronted with what will
obviously be a necessarily-incomplete "solution"... simply because one will
left having to postulate a "black box" (a set of things where, like that
cartoon depicts, "Something magic happens", which, although the 3-D geometry
not been carried through, never-the-less, activates the effectors in a way
commensurate with the 3-D geometry inherent in the external environment.) Do
follow? It's not sufficient to say anything about anything within the
system without placing it solidly within this global
necessity... in the past, folks have scratched their heads with respect to
and muttered, "humunculus"... and there it was, the "black box" where the
"magic" happens unexplainedly... and so nothing "fit together".

The "stepping-back-to-go-forward" exercise, above, is an absolute
for everything else.

> > > Theoretical models of associative memory are very
> > > robust with respect to the choise of plasticity
> > > mechanism, and a number of different mechanisms
> > > will do the job equally well. Neurons do also
> > > express different types of plasticities, not just
> > > linear scaling of synaptic weights.
> >
> > Of course, it's kind of hard to "draw a picture" using only
> "straight lines".
> >
> I'm not sure what is meant here.

I was referring to the stuff of the 3-D-geometry-preservation... for
linearly-graded activations would allow only very-crude effector actions.
effector actions that we observe require myriad types of "brush strokes" to
"paint". Do you follow? Wiggle your fingers... manipulate an object with one
while gently exploring that hand via touch (with the other hand) and
vision... I
know this, too, doesn't sound like Neuroscience, but it's all a necessary
to grasping the nature of the spectrum (the storm, really) of activation
occurs internally. (In these things, I'm carrying the discussion all the way
to fundamentals that were pointed out by Torsten and Wiesel in their
investigations of vision... and addressing the question of why, when one
visual cortex, for instance, one does not necessarily witness activation
"looks like" an image of the momentary visual stimulus set... rather, one
sees a
"patch work"... (many geometrically-distorted "patch works") it's relatively
the same everywhere within the nervous system,
and the problem reduces to explaining how such readily-observed "patch
rigorously correspond to the 3-D geometry of the external environment with
respect to which the effectors must act rigorously.

=Only= after getting all of the above firmly in grasp, can =anything= be
about "memory".

And, although I've barely discussed sensory dynamics, with what's here, the
nature of the realm in which "memory" is constrained concisely. Whatever
the molecular mechanism, the existence of which, because of the fact of
progressive-establishment, we can postulate without explicating completely,
=must= posses the physical capacity for causing the ongoing activation state
be minimal, to preserve the 3-D geometry, and to reflect the asymmetry of
necessary effector activations.

So in this, activation of individual neruons that are observed to be
are just particular harmonics within the overall 3-D-geometry whole... they
not, at all, any more-"special" than are momentarily relatively-quiescent

It's just that one cannot begin to approach "memory" without carrying all of
"lower-"evel" stuff right through one's discussion.

> There is a great deal of complexity
> associated with the LTP phenomenon. I've read discussions of everything
> NMDA receptors, calcium/calmodulin dependent protein kinases (which might
> impact synapsin presynaptically and have other effects postsynaptically),
> synthase (which interestingly is related to an epithelial enzyme and also
> an enzyme that mediates neutrophil/macrophage activity), and metabotropic
> glutamate receptors that could act via an inositol (or diacylglycerol?)
> pathway. I've posted about a study that looks at cell adhesion molecules.
> With all these various components implicated, it is hard (for me) to
> at a good signal/noise ratio wrt LTP. Perhaps this will subside as I delve

> deeper into all central and ancillary issues. With  an integrated approach

> that includes all the putative components in LTP (a phenomenon marginally
> related perhaps to memory processes in the hippocampus) it is quite hard
> draw straight lines. It is easier to pick out specific components
> receptors and protein kinases) and ignore the other stuff. I am interested
> the cell adhesion molecule aspects though.

Perhaps because I earn my sustenance as a computer programmer, in which
I've witnessed the transition from magnetic-core "memory" and various
magnetic-disk "memories", to bubble "memory", to on-chip "memory", and
because my
view has been from the perspective of energy-content and configuration which

enable the storage of energy which translates into a computer's capacity for

doing the physical work that memory-"addressing" entails, I see the
molecular-embodiment, while of high-significance, as being "moot"... any
=must= be as the capacity for for exerting physical force, at a particular
within the ongoing global activation state, that embodies the necessary 3-D
geometry. In the brain, this occurs, of course, as a function of
hugely-distributed dynamics,
with "memory", itself, being commensurately distributed (Karl Lashley's
awesomely-Beautiful 30-year's work).
Check it out, any proposed mechanism of "memory" =must= fall within
this constraint, or the global system cannot process information. So, with
additional constraints which order everything rigorously, it's as you say,

> > > There is no reason to believe that Altzheimer patients
> > > have impaired memory because they lack LTP. If they
> > > do lack LTP, one should rather say that they are
> > > impaired on synaptic plasticity.
> >
> > This can't be said... all that can be said is the hypothesis
> must be tested
> > if anything's to be said.
> >
> The transgenic study I've looked at ties an amyloid protein expression to
> deficits in LTP.

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