neurodudes

As you know, here at Neurodudes, we’re always interested in seeing how people are applying results from neuroscience to areas outside of academic neuroscience. Today, I got the following in my inbox:

Special Lecture
BRAIN PLASTICITY IN AGING
Wednesday, February 1, 2006
10:00 am 46-4062
Bonnie Connor, Ph.D., Laila Spina, Psy.D., and Natasha Belfor, Ph.D.
Posit Science Corporation
San Francisco, CA

Leading me to the natural question: What is Posit Science Corp? Well, here is their website. They seem to be a company focused on keeping mental abilities sharp. To that end, they have lead seminars and sell computer programs based on aging research results.

I haven’t looked over their website in detail but they do seem to have a lot of information on the science behind their techniques and Mike Merzenich is their Chief Scientist. (There’s quite a few names you might recognize on their list of advisors and consultants.)

The nice NYT article on the function of sleep follows on a recent NIH-funded Nature insight series.

Some interesting facts from the NYT article:

• Sleep patterns vary greatly. Some bats sleep 20 hours, giraffes get 2 hours. (hmmm… grad students might be evolving toward giraffes…)
• Sleep has recently been found to occur in invertebrates too. Alternatively stated: Sleep is evolutionarily very old.
• Slow wave sleep is also found in fruit flies. (Divergence from fruit flies for us was 600 million years ago.)
• Some people don’t have any REM sleep. Behaviorally, these people are entirely normal, implying that it’s purpose might not be as obvious as one had thought (ie. required for the preservation of new memories, etc.)
• If you put a bunch of ducks in a row, the ones on the inside will sleep more often with both eyes closed. The ones on the outside will sleep with one eye open and it is (always?) the eye facing outward from the huddle. They are able to “sleep” one half of the brain at a time and, apparently, this sleeping with one eye open was lost in higher mammalian evolution. Fascinating.

This article is about efforts by six teams to develop a hippocampal prothesis by monitoring the input/output transformations performed by the hippocampus in slice, and then creating an electronic device to mimic them.

The article quotes noted memory researchers Howard Eichenbaum and Norbert Fortin who seem to approve of the methodology.

Jimbo, Tateno, and Robinson did a network plasticity experiment using cultured networks and a multi-electrode array.

They determine the effect of a tetanus at one electrode in a network on the network. Specifically, they look at how the tetanus potentiates or depresses the ability of a test pulse at another electrode to evoke spike trains at various neurons across the network.

They grew cultures on a MEA for a month. They stimulated each electrode in succession with a test pulse. They recorded the response at all electrodes after each test pulse. They used spike sorting to identify the reponses of individual neurons out of the electrode traces. They found that the network’s response to a given test pulse was reproducable for about 50ms after the test pulse.

Then they applied a strong stimulus (a tetanus) to a single electrode (to make it learn ). After that they re-characterized the network’s responses to test pulses at every site.

They found that some electrode sites became more potent (“potentiated response”) after the tetanus was applied. This means that, when a test pulse was applied to this electrode site, neurons in all areas of the network responded either the same, or more strongly than they had before the tetanus.

Other sites became less potent (“depressed response”) after the tetanus was applied.

Surprisingly, it was very rare for any given electrode site to become better at stimulating some neurons and worse at stimulating others as a result of the tetanus.

What determined which electrode sites became potentiated and which ones became depressed? The tetanus potentiated electrodes which evoked spike trains that tended to contain spikes which were within 40ms of the spike trains evoked by the tetanus electrode, and depressed others. That is, it potentiated sites which evoked patterns similar to the patterns evoked by the tetanus site.

However, the spike trains evoked by both potentiated and depressed neurons became more synchronized with the tetanus electrode after applying the tetanus.

See page 5 of “Distributed processing in cultured neuronal networks” for another review of this work.

See this NeuroWiki page for more details (the strange {{}} over there are because we will soon have footnotes).

Jimbo, Y., Tateno, T., and Robinson, H. P. C.,
Simultaneous Induction of Pathway-Specific Potentiation and Depression in Networks of Cortical Neurons. Biophysical Journal, 1999. 76: p. 670-678.

For those with theoretical interests with respect to machine learning flavored AI, the ML Theory blog run by John Langford is highly recommended. Though recently started, Langford and others have so far been doing an excellent job of commenting on both the science and culture of theoretical learning research.

Scientific Clearing House: Mind enhancing drugs

Apparently, CX717, an ampakine developed by Cortex Pharmaceuticals, shows some signs of preventing the cognitive impairment brought on by sleep deprivation. The original study in PLoS Biology (news & views) was done with monkeys.

Neuroimaging data of different brain areas fit to a Rescorla-Wagner model show that different cortical areas integrate stimulus changes over different time intervals. The result itself probably isn’t that shocking but I liked the nice combination of theory and experiment.

From the July 21 Neuron:

Formal Learning Theory Dissociates Brain Regions with Different Temporal Integration

Jan Gläscher and Christian Büchel

Learning can be characterized as the extraction of reliable predictions about stimulus occurrences from past experience. In two experiments, we investigated the interval of temporal integration of previous learning trials in different brain regions using implicit and explicit Pavlovian fear conditioning with a dynamically changing reinforcement regime in an experimental setting. With formal learning theory (the Rescorla-Wagner model), temporal integration is characterized by the learning rate. Using fMRI and this theoretical framework, we are able to distinguish between learning-related brain regions that show long temporal integration (e.g., amygdala) and higher perceptual regions that integrate only over a short period of time (e.g., fusiform face area, parahippocampal place area). This approach allows for the investigation of learning-related changes in brain activation, as it can dissociate brain areas that differ with respect to their integration of past learning experiences by either computing long-term outcome predictions or instantaneous reinforcement expectancies.

How does this relate to Hawkins’s idea that all cortex implements the same underlying “algorithm”? Is the integration time constant (or, in RW terms, the learning rate) tuned differently by different inputs?

NEUROSCIENCE: Preventing Alzheimer’s: A Lifelong Commitment? — Marx 309 (5736): 864 — Science

Some quotes of interest:

For example, a 1997 study of 642 elderly people, conducted by Denis Evans of Rush Presbyterian-St. Luke’s Medical Center in Chicago and his colleagues, found that each year of education reduces a person’s risk of Alzheimer’s disease by 17%.

[...]

As in other studies, Snowdon and his colleagues found that high education levels seem to protect against Alzheimer’s disease. The researchers originally thought that this supported the idea that more education leads to a higher cognitive reserve. But analysis of biographical essays the sisters had written when they entered the convent, usually in their early 20s, pointed in a different direction. The early writings, Snowdon says, were an even better predictor of who would get Alzheimer’s disease than education level. “Those who had the lowest linguistic skills at age 22 had a very high risk of Alzheimer’s,” Snowdon says. Indeed, most of the cases occurred in the nuns whose essays put them in the bottom third on the linguistic ability scale.

[...]

A few years ago, Arthur Kramer of the University of Illinois, Urbana-Champaign (UIUC), and his colleagues performed a meta-analysis of 18 trials involving adults between the ages of 55 and 80 that explored the effects of physical exercise on performance of various cognitive tasks. They concluded that the answer to the question, “Does aerobic exercise enhance cognition?” was an “unequivocal yes.”

[...]

As reported in the April issue of the American Journal of Epidemiology, study members who engaged in four or more physical activities, which could be anything from gardening to jogging or biking, had about half the risk of dementia as that of participants who engaged in one or none. The effect was primarily seen, however, in persons who did not carry a gene variant called ApoE4 that’s known to increase Alzheimer’s risk. In the ApoE4-endowed population at least, genetics seems to trump activity.

[...]

Another possibility is that exercise turns up production of proteins that stimulate neuronal growth. About 10 years ago, Carl Cotman’s team at UC Irvine, found that the brains of rats who ran voluntarily on a wheel show increases in one such factor, BDNF (for brain-derived neurotrophic factor). The increase was particularly strong in the hippocampus, an area involved in learning and memory that’s hard-hit by Alzheimer’s disease.

Edge magazine asked people, “What do you believe is true even though you cannot prove it?”

Terrence Sejnowski’s answer was that, “the substrate of really old memories is located not inside cells [or in synaptic strengths], but outside cells, in the extracellular space.”
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Last summer, I began to make an online mini-bibliography on neocortical synaptic plasticity. It currently contains over 160 citations divided into over 35 cross-linked subtopic listings.
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