[Murg] Connectionists: NEURON Summer Course registration deadline approaching (fwd from ted.carnevale@yale.edu)

[Eugen Leitl]

On Thu, Apr 07, 2005 at 12:49:01PM -0400, cat13 at illrepute.org wrote:

> > It's not just the segmentation issue, we don't know the properties of
> > whatever pieces of neuroanatomy we can segment. This isn't a worm, where
> > everything is known and doesn't need labels, since in standard
> > locations/connectivity.
> 
> What information IS available for turning these images into a working
> model of anything?

We can probably infer some of the properties of the shapes by assembling the complete
3d model from multiple sections (notice that inter-slice stride is
considerable).  

But we'll need to go beyond TEM to obtain these properties.
 
> And what missing information would be most useful to have?

As a random example, http://www.sciencemag.org/cgi/content/full/308/5718/83

Postsynaptic Receptor Trafficking Underlying a Form of Associative Learning
Simon Rumpel,1 Joseph LeDoux,2 Anthony Zador,1 Roberto Malinow1*

To elucidate molecular, cellular, and circuit changes that occur in the brain
during learning, we investigated the role of a glutamate receptor subtype in
fear conditioning. In this form of learning, animals associate two stimuli,
such as a tone and a shock. Here we report that fear conditioning drives
AMPA-type glutamate receptors into the synapse of a large fraction of
postsynaptic neurons in the lateral amygdala, a brain structure essential for
this learning process. Furthermore, memory was reduced if AMPA receptor
synaptic incorporation was blocked in as few as 10 to 20% of lateral amygdala
neurons. Thus, the encoding of memories in the lateral amygdala is mediated
by AMPA receptor trafficking, is widely distributed, and displays little
redundancy.

1 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2 New York University, New York, NY 10003, USA.

* To whom correspondence should be addressed. E-mail: malinow at cshl.edu

Animals continually adapt their behavior in response to changes in the
environment. It has long been held that selective modifications in synaptic
efficacy represent the physical substrate for this behavioral plasticity (1,
2). Long-term potentiation (LTP), a cellular model of synaptic plasticity,
has emerged as a leading candidate mechanism underlying associative forms of
learning in the central nervous system (3–12). Much is now known about
the molecular mechanisms during LTP that translate a brief change in
electrical activity patterns to a modification in synaptic efficacy
(13–23). Recent studies indicate that synaptic addition of GluR1
subunit–containing AMPA-type glutamate receptors (GluR1-receptors)
mediates the synaptic strengthening observed during LTP (24, 25). An
attractive proposal is that a learning-driven increase in GluR1-receptors at
a selected group of synapses underlies associative memory.

-- 
Eugen* Leitl <a href="http://leitl.org">leitl</a>
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