[Comp-neuro] Re: Attractors, variability and noise
bower at uthscsa.edu
Wed Aug 13 18:47:24 CEST 2008
> As I understand the other end of the spectrum, we construct
> increasingly realistic models and end up with a simulated brain
> without a real understanding of how it works, which makes no sense
> to me. Understanding is what we're after, and that understanding
> can only reside in the brains of the population of scientists, not
> in their models.
> I suspect that I have created a straw man here, but I'm curious to
> what extent I've abused your position.
Haven't abused at all -- with one big exception -- realistic models
are more likely to tell you how things work, than are models in which
'how things work' is assumed. In our experience, realistic modeling
has consistently and steadfastly told us things that we didn't know
before - problem is, those things fly in the face of many of the
current 'theories" operating in the parts of the brain I study, making
the publication of papers, getting grants, etc, much more difficult.
BTW, almost every time, the models have also made it clear that I was
wrong in how I was thinking about the system:
The most recent example for those that are interested:
Santamaria, F., Tripp, P., and Bower, J.M. 2007 Feed-forward
inhibition controls the spread of granule cell induced Purkinje cell
activity in the cerebellar cortex. J. Neurophysiol. 97: 248-263.
Despite complaints by the reviewers, both the introduction the first
part of the results section of this paper and the discussion, make it
clear that the mechanism I had thought for 20 years was responsible
for a particular physiological property of this circuit, was wrong.
One of the paper's reviewers, complaining about the length of the
paper, requested that we cut that part out, and just state what we now
know to be true - I responded that I have no more certainty that what
we now think is the case is true, than I did before -- it is just a
new platform to move forward.
Why is this interesting in the larger sense? (sorry to go into the
details, but in biology the details matter). Because our current
models combined with our physiological results continue to suggest
that the 150,000 excitatory parallel fiber inputs to cerebellar
Purkinje cells actually have no direct influence on the output of the
neuron. What's wrong with that? Every top down model of cerebellar
function assumes they do -- How come they continue to believe this?
Because all the models that manifest these top down "ideas" ,
implement Purkinje cells as integrate and fire "pattern recognizers".
It would be hard to imagine a cell in the nervous system less likely
to be an IF neuron than the Purkinje cell.
Is it potentially significant for thinking about the rest of the brain
that some, perhaps many, possibly even MOST of the excitatory
connections on neurons may not have anything to do with their direct
output? -- seems to me it could be.
How many abstract models of brain function assume excitatory synapses
sum to produce outputs? -- lots, even most. How many neural network
models are built on this assumption? almost all.
Is the right approach then to build models that are so abstract that
these details don't matter? How can the nervous system tell you you
are wrong if you do?
Do MOST cerebellar physiologists, modelers, theorists, think this view
of cerebellar Purkinje cells is crazy? -- yes -- Why? they have too
much invested in other ideas.
Is the Purkinje cell model available for others to examine, test,
include in their models, explore, refute, etc? you bet -- How many
Glory days - this is starting to happen. :-)
In fact, it fills me with a great sense of hope that the Purkinje cell
model is now being used in multiple laboratories around the world,
MOST not connected in any way to my laboratory, as a basis for further
study. AND -- importantly, not all of those modelers reach the same
conclusions we do -- BUT, equally importantly, we now have a
quantiative substrate on which to discuss, argue and resolve. THAT is
progress in my view, WHATEVER the outcome. Most of the time in
neuroscience (as manifest abudendently in this ongoing conversation)
we can't even agree on the definitions (a convenient way to avoid
conflict -- and at the same time progress).
With the Purkinje cell, we can argue about K channel conductances
(which were way off in our initial models), and other things that can
actually be experimentally tested.
In fact, I am extremely proud that the PC model has even been
converted to Neuron for use in other laboratories, including several
who don't believe what I believe at all.
This is one of the first times in history that a complex realistic
model has spread across labs and opinions -- and speaks very well for
the future - this is what the GENESIS project was about to begin with
-- and now, more than 20 years later, it is starting to happen, not
only with GENESIS but through Neuro-DB built by Michael Hines and the
Neuron group at Yale as well.
There is hope
Dr. James M. Bower Ph.D.
Professor of Computational Neuroscience
Research Imaging Center
University of Texas Health Science Center -
- San Antonio
8403 Floyd Curl Drive
San Antonio Texas 78284-6240
Main Number: 210- 567-8100
Fax: 210 567-8152
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