[From Rick Marken (2004.05.278.1200)]
Marc Abrams (2004.05.28.0621)]
Rick there are no definitive answers yet as to how the physiology of control
Of course not. I'm guessing about what _might_ be the physiological basis of
control based on what I know about control and physiology. The idea that
efferent neurons above the spinal-motor level function as references for
afferent input is a hypothesis, but I think, a reasonable one based on what
we know about the functional components of a control system and the
functional components of the nervous system. I would like to see research to
test this hypothesis. If it turns out that the hypothesis is wrong then we'd
have to come up with another hypothesis regarding the physiological basis of
control. I can't imagine what that would be right now but we don't know that
we need an alternative yet. But if you already have alternative, then that's
great. I'd like to hear what it is. Neuroscientists could then do research
on both hypotheses in parallel.
I am not arguing for a specific point of view. I am arguing for a
discussion of several possible points of view.
Maybe this is one of our problems. I'm not interested in alternative "points
of view" about the physiological basis of control. I'm interested in
alternative hypotheses (in the form of models) about the physiological
architecture underlying control. Bill Powers, in B:CP, proposed what I think
is a very reasonable hypothesis about the physiological basis of control. He
described this hypothesis in some detail in terms of well known features of
the anatomy (organization of neurons) and physiology (neural firing rates)
of the nervous system. If you have an alternative hypothesis regarding the
physiological basis of control I would very much like to see it. But I would
like to see it described in terms of anatomical and physiological diagrams
so I can compare it to Bill's model.
Lets get this stuff out on the table.
Let's indeed. What I would like to see placed on the table are hypotheses
about the physiological basis of control that are described at _at least_
the level of detail as the hypothesis described in B:CP.
How can we ever possibly understand the physiological mechanisms behind the
control model if we don't try cut through the muck and glut of BS that is
currently going on in the various fields relevant to PCT if we refuse to
acknowledge that the model needs work
We all assume that the physiological model of control proposed in B:CP is
tentative: it needs work!! But we can't know what work it needs until the
model is tested. That means physiological tests to see, for example, whether
variations in the firing rates of particular efferent neural signals result
in concomitant changes in the firing rates of corresponding afferent signals
(in an intact organism that can act to control the perception represented by
the afferent signal). Perhaps there are such studies and they show that this
kind of efferent/afferent signal matching doesn't occur. It would be
interesting to find such studies.
Bill thought that people would take the
model as a starting point and do the necessary research to find the 'real'
definitive answers, but what actually happened was that Bill felt he was
forced to defend his position and as such, instead of embracing the vision he
extolled in B:CP dug a very deep defensive moat to protect himself from what
he perceived to be people out to 'get him'.
I don't see this at all. I think Bill has been defending a correct
understanding of his theory and demanding only that it be evaluated using
the methods of science. This kind of defense has been necessary because
most criticisms of the theory have been nothing more than opinions based on
ignorance and prior agendas. Bill encourages proper tests of the theory and
if these tests produce results that require revision of the theory Bill will
revise it (as he did when I presented data long ago showing that a transport
lag had to be added to the control loop in order to account for tracking
data in which the disturbance was created by an active agent rather than by
a passive process - the "Marken effect", which I really should write a paper
on) rather than defend it.
I am a firm believer in PCT
Like Bill Powers, I am not a big fan of belief. I would be much happier if
you were a skeptic regarding PCT and that you knew how to put your
skepticism to work by _testing_ PCT to see if it is worth believing in at
all.
Finally, let me give you the answer I have for my questions
Great.
1)You seem to be defining 'levels' by how 'central' they are too something.
Central to what?
I asked this question because I find the PCT hierarchy ambiguous. It purports
to represent location (central, peripheral) _and_ functionality
(relationships, systems, etc.) So again, I ask you, which is it?
The functional hierarchy (such as the one implemented in my spreadsheet)
says nothing about the spatial organization of the systems involved. The
anatomy and functionality of the nervous system suggests that, if the NS is
a hierarchy of control systems, it is almos certainly arranged anatomically
with the highest levels in the cerebral cortex, lower levels in the thalamus
and celebellum, still lower levels in the medulla and spinal ganglia and the
lowest level connecting to peripheral sensory and motor organs.
But it really doesn't matter.
Rats. I wasted a whole paragraph on something that doesn't matter anyway;-)
Perceptions, as defined by current neuroscientific standards
are not constructed as they are purported to in the HPCT hierarchy.
PCT doesn't say much about _how_ perceptions are constructed other than that
this construction is probably carried out by a neural network that
transforms multiple sensory inputs into a scalar variable that is the
perceptual variable. This general conception of the process is consistent
with the functional and neurophysiological models of perception with which I
am familiar, such as the Hubel-Weisel receptive field model of "feature"
perception, lateral inhibition models of edge perception, perceptron-type
models of optical character recognition, etc. I think the main difference
between the PCT model of perception and these others is that the perceptual
signal in PCT is continuous rather than logical (yes/no).
I believe memory and emotions affect and are
affected by every function in the model and most importantly our perceptions
and reference levels.
Beliefs are far less interesting to me than models and data. With a little
effort I can believe that memory and emotions affect perceptions and
reference values. But what do I do now? Go worship at the church of memory
and emotion? My inclination is to test this notion. But in order to test it
I have to know what it means. I have to know how memory and emotion are
defined; how they are measured; how they contribute to the behavior of a
model of control. Once I know this, I can test the model. Bill Powers has
presented a model that shows how memory and emotion can be included in a
model of control. Bill has done some testing of the memory model; no one I
know of has done any testing of the emotion model. Before I start working on
your ideas about memory and emotion I would have to see what your model is
and I would also have to see evidence that shows that the PCT model of
memory and emotion (such as it is) is wrong.
2) how does this hierarchy reflect the levels in PCT?
Good question. I don't have a clue what you have in mind. Could you elaborate
on how 'centrality' has anything to do with 'relationships' or
'configurations'?
I don't think it has anything to do with it.
Forgive me if I find your opinion a tad less convincing that that 5 or so
chapters in B:CP that describe physiological evidence for a relationship
between Bill's proposed levels of perceptual control and anatomical levels
of the nervous system.
3) Where and how do the 'efferent' signals get 'compared'? And too [sic] what?
Again, I don't have a clue as to what you're talking about here. There are
over 50 different types of neurons and there is some question now as to how
much info is communicated 'chemically' vs. 'electronically'. Neuronal
electronic communication is over _very_, very short distances. 'Signals' as
envisioned in B:CP just don't exist in our nervous system.
I find this very hard to believe. Where did these signals go? Last I heard,
single cell recordings of neural firing show that neurons fire at a rate
proportional to stimulation at the cell body. Aren't they finding these
signals anymore? I know they were finding them as late as 2000 when Peter
Cariani reported on them at the Boston CSG meeting. Peter thought it was not
only the rate of firing but the temporal pattern of firing that constituted
the neural signal. If that's true it would require some significant changes
in the physiological model of control. In fact, that might be a nice thing
for you to work on with your new found mathematical skills. Build a control
system that operates based on signals that vary in spectral composition
rather than simply in rate of firing.
But _PLEASE_ Rick, do not take this a condemnation of PCT.
Of course I don't.
Bill's notion of signaling in B:CP is called 'labeled lines', and is outdated
and has been largely discredited by the neuroscientific community
So what do they use instead? What's the correct model?
And discrediting is what is done in politics. Disproving (rejecting by
scientific test) is what is done in science. So if all that has been done in
neuroscience is discrediting of the PCT model of neural signal transmission
than I'm not interested. The idea that behavior is purposeful was (and still
largely is) discredited in psychology but, it turns out, behavior _is_
purposeful. If the PCT model of neural signals has been disproved by
neuroscience then it should be a simple matter to explain the evidence that
disproves it.
It seems the frequencies change as they travel from neuron to neuron, or
cluster to cluster.
That is certainly not inconsistent with the PCT model of neural signals. We
expect signal rate changes as signals travel from error signal nurons to
reference signal neurons to output neurons - and the same would be expected
coming up through the perceptual hierarchy.
4) How is an 'error' signal different than a reference signal?
I think this is a very important question and one that needs to be answered
empirically by finding and understanding how control mechanisms work in the
body. I have studied a couple of physiological control systems and neither one
adhered to the concept of the PCT perception, reference, comparator, error. In
the two case I've studied both had hard wired 'reference levels' but had
different modes and mechanisms of operation. One system had the
characteristics of 'bistabilty'. That is, the 'reference level' could and did
switch between a finite number of levels all seemingly dependent on what was
perceived. The other system had a seemingly simple on/off switch. If the
perceived gradient of a chemical in the environment was at a certain level a
chain reaction would ensue and a process would take place. If not it wouldn't.
Now this is interesting. How about describing the "bistable" system (for
starters) in some detail. What variable is the system controlling? What's
this business about the reference level switching based on perception? How
about a diagram of the system? How did they determine which component of the
system was specifying a reference level? A perception? Was the system
observed under conditions in which it could control successfully? What is
their neural model of the control process?
5)Are all 'efferent' neurons 'reference' neurons? If not, what do the other
'efferent' neurons do?
I think this whole notion needs to be reconsidered.
That's fine. But the question is _why_. What is the evidence that leads you
to reject this notion? Better yet, please describe what you think is the
better notion (using anatomical diagrams and physiological evidence).
Regards
Rick
···
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Richard S. Marken
MindReadings.com
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