The Mathematics of Neuroscience 51
eldavojohn writes "An academic paper on math [PDF] has been released by Paul Bressloff, resulting in much ado about the mathematical modeling of the brain's memory storage. The paper deals with specific receptors called AMPA and how memories are held while synapses still fire. Scientific American is running a more detailed report on the subject." From the article "At any given time, some AMPA receptors are moving inside the nerve cell where they are unable to receive signals. But to maintain memory, a number of AMPA receptors are anchored in place with what are known as scaffolding proteins, Bressloff said. The computer models examined how many AMPA receptors are anchored at the receiving area on the surface as opposed to those found elsewhere in the nerve cell. The more AMPA receptors that are anchored in place, the stronger the synapse."
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Also, just because you can reduce neurons to a simplified model, it doesn't mean that these models, or the thing they're modeling, are
Theoreticians vs. experimentalists (Score:3, Informative)
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Collaboration (Score:2)
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So, the Izhikevich-type neurons...I actually used those once, a few years ago, when I was attempting to make a model of oscillations in the locust antennal lobe. I actually started with a Wil
How many neurons are in Drosophila? (Score:2)
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The Drosophila CNS is not like C. elegans, where every single neuron is specified, but in some brain regions it's close to that. Also, there are not very many neurons--I think something like 250,000 in the entire brain, and often as few as tens to hundreds of a certain class of neurons in a particular struc
*rimshot* (Score:2)
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I concur that i
Detailed models of neurons (Score:2)
I have not been personally involved in any detailed models of neurons, but there are models out there of single neurons with thousands of compartments. These definitely don't fit the "black box" description, IMO, and I think they do quite a good job of modeling the behavior of the neurons they're designed to model. I don't know if one has been worked out for a cortical pyramidal cell, but I do know they work quite well for hippocampal pyramidal cells, and I'd be very surprised if they hadn't been worked out
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Yes I do know about the hippocampal models, and yes t
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Wha? (Score:5, Funny)
Prof. Farnsworth: Same thing I teach every semester: The Mathematics of Quantum Neutrino Fields. I made up the title so that no student would dare take it.
Fry: Mathematics of wanton burrito meals. I'll be there!
Prof. Farnsworth: Please, Fry, I don't know how to teach; I'm a professor!
I can't remember (Score:1)
It really makes you think.
Re: I can't remember (Score:2)
I doubt it. They don't tend to get their panties in a bunch over anything else coming out of neuroscience. (Though perhaps only because their oblivious to it. Maybe the next person who wants to compete for stardom in the anti-science profession will adopt this as his whipping horse; too much competition these days in the evolution-denial movement.)
You do encounter a lot of dyed-in-the-wool dualists on the 'net who should bal
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I don't know much about it. Apparently 'they' have experimented with people playing a game designed to pit your greed against your sense of fair play, and people's decisions swing way in one direction when part of their brain is exposed to some kind of magnetic field while playing.
I read something about it very recently, but can't recall where.
TMS (Score:2)
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imagine what it has to do with religion in the mind of a person who regards materialistic
reductionism as a refutation of religion, but I can't imagine how anyone could take
such a view seriously, and simultaneously consider themselves intellectually honest.
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This "ol' religious community" you speak of is only the religious right. I know of plenty of religious people who don't have anything against neuroscience as long as the research is ethical (i.e. no human babies chopped up). I'm not religious myself, so I don't understand their rationales and can't explain how they reconcile this matter of mind and soul.
P.S. It's "reckon" not "recon".
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It is 'recon' I was trying to make a joke.. Apparently references to Loradidine are dead.
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I only ever have religious feelings, like I used to have when I was a kid, at one time, and that is during epileptic seizures. Along with a lot of other inappropriate emotions. Some nuclei in the limbic system get fried by the synchronized currents. Of course I'm always pretty out of it at that point, but that's about what you'd expect.
old news and/or nsufficient evidence (Score:5, Interesting)
none of this stuff is particularly new. here's a brief summary of the first linked-to article:
integrate-and-fire models are extremely simple -- the idea (as implied by their name) is that this neuron model spikes if the membrane voltage passes some set threshold, and otherwise doesn't fire. In response to input current, the cell's membrane voltage charges (depolarizes) or decays (hyperpolarizes) according to exponential time constants. the other spiking models discussed are similarily oversimplified. (these simple neuronal models can be useful, for example in models of neural networks.)
the second article (the main one) is extemely vague on (a) how their findings were verified in actual neurons and (b) whether their model was borne out in actual neurons. i love computational neuroscience, and i think it's an extremely useful tool. one major downside with almost all computational models, however, is that they rely on assumptions that the designers can't prove. designing these models is often an iterative process, where (1) experiments inspire creation of a new model, (2) the model simulates a new condition during which new predictions are made, and (3) new experiments are performed which require adjusting the model or running more simulations. thus, to conclude (as this article appears to) that the authors have "proved proved that the presence of more scaffolding proteins available at the far downstream end of the neuron (and into the synapse) to AMPA receptors increased during LTP..." is misleading, given the dirth of evidence presented in the article.
if scaffolding proteins end up being verified as the mechanism by which AMPA receptors are anchored in the way the authors propose, that might be pretty interesting -- but clearly much more work needs to be done to verify that this is actually the case. the idea that AMPA receptors are promoted during LTP (increasing synaptic strength) and "demoted" during LTD (decreasing synaptic strength) is quite old (for example, see The Cognitive Neuroscience of Memory, published in 2002, by Howard Eichenbaum for a review).
Re:old news and/or nsufficient evidence (Score:5, Informative)
I think this is the key. Laypeople think that the reason we don't understand the brain is because it's too complicated. It is complicated, but the main difficulty is the inconvenience of the brain as an experimental system. It's very hard to see what's going on inside a brain without damaging it so it doesn't work any more, so we're stuck using experimental tools that answer the questions we can answer instead of the questions we want to answer. So basically what I think you're saying (and I agree) is that the problem with modeling approaches is that the data isn't there to back them up. I would argue that means the real problem is not with the modeling, but with the experimental side (and I say this as an experimentalist, so it isn't meant in any derogatory way).
The solution is easy.. (Score:2, Insightful)
It's called threading..
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Research abstract; more info (Score:5, Interesting)
Biophysical Model of AMPA Receptor Trafficking and Its Regulation during Long-Term Potentiation/Long-Term Depression [jneurosci.org]
AMPA receptors mediate the majority of fast excitatory synaptic transmission in the CNS, and evidence suggests that AMPA receptor trafficking regulates synaptic strength, a phenomenon implicated in learning and memory. There are two major mechanisms of AMPA receptor trafficking: exocytic/endocytic exchange of surface receptors with intracellular receptor pools, and the lateral diffusion or hopping of surface receptors between the postsynaptic density and the surrounding extrasynaptic membrane. In this paper, we present a biophysical model of these trafficking mechanisms under basal conditions and during the expression of long-term potentiation (LTP) and depression (LTD). We show how our model reproduces a wide range of physiological data, and use this to make predictions regarding possible targets of second-messenger pathways activated during the induction phase of LTP/LTD.
Computational neuroscience is a great topic. If you're interested in learning more about it, there's a nice book by Gerstner & Kistler called Spiking Neuron Models, which can be purchased hard-copy or downloaded for free online [diwww.epfl.ch]. The wikipedia page [wikipedia.org] is also pretty good, with plenty of links to fun neural simulation software.
(And yes, I Am A Computational Neuroscientist... or at least I'm in a computational neuroscience grad program
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This is correct as the first link in the post is not directly concerned with the paper. I actually know Paul Bressloff pretty well and his work is pretty exciting. Of course the next step is biological validation of the data and we've talked a bit about how to go there. The trick will be to find funding in this current political climate for this work.....
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"Academic Paper"?? (Score:1, Informative)
Fromt the what .dept? (Score:2)
My neural network actually hurt trying to decipher that...
memory in part (Score:3, Informative)
Nobel-prize winner Kandel elucidated a mechanism of memory with the gill reflex in Aplysia: the response to a water jet on the gill which could lead to long term- and short term memory. Two possible 'directions' of memory are habituation and sensitization.
Habituation is a downregulation of the response to a signal. In snails the response of the gill reflex will decrease over time, just like you forget a source of noise if you hear it long enough.
Sensitization is a mechanism in which the response to a signal is increased. The response of the gill reflex can be increased when it is coupled by another stimulation. For instance a small electrical shock on the head. This model was already known from Pavlov's studies on dogs: a bell can induce a 'food' response when previously associated with food. The aplysia model was more suitable for study on a cellular scale, however.
to quote the article this is how communication between neurons work:
Here I should mention the transmission at a synapse involves many signals, not just one. The synapse is a location that is carefully regulated. Sensitization and habituation occur at the synapse. The synapse changes physiologically in these events.
This AMPA receptor is one of the receptors that is associated with the learning response. It isn't the only receptor, though, and signals in the synapse are very complex and regulated through many signaling pathways.
Here's more about memory:
http://www.journals.royalsoc.ac.uk/(vzapqd45k3ktb
http://www.jneurosci.org/cgi/content/full/25/23/5
Hype out of nothing + Stealing other people's work (Score:2, Informative)
(1) The topic treated is old stuff, there is plenty of evidence for it, for instance see Roberto Malinow's beautiful work on this subject. Unfortunately the model does not add anything.
(2) I have no idea how they got themselves into Scientific American, clearly its quality is going down.
(2) The posted link is to a text-book with little relevance to the actual research. However, I was very surprised to find an unattributed figure in the text made
Re:Hype out of nothing + Stealing other people's w (Score:2)
BT (Score:1)
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