Motor Interneurons That Inhibit Sensory Neurons

How do crickets know when they are chirping?

These questions appear to be answered with the discovery of a motor interneuron in the cricket that is resposible for “corallary discharge” or forwarding neural signals from motor systems to sensory systems. By inhibiting auditory neurons during chirping, the animal can “counter the expected, self-generated sensory feedback”.

Over at the synapse blog, it is pointed out that the cerebellum may have this function in vertebrates.

EEG study of states of mind conducive to storing memories

“Scans of brain activity, published online in the journal Nature Neuroscience, indicate that the brain can actually get into the ‘right frame of mind’ to store new information and that we perform at our best if the brain is active not only at the moment we get new information but also in the seconds before.
Tests showed that the brain’s electrical activity differed after the cue question and before the word was presented and this was linked to whether the subject would remember or forget the word in a later unexpected memory test. If the electrical activity maintained a high level over frontal parts of the scalp just before the word was shown, then it was likely that the subject would remember the word up to 50 minutes later – and after doing a series of other word tests. On the other hand, if the voltage was lower, the subjects were less likely to remember the word.”

(from the press release)

Leun J. Otten, Richard N. A. Henson & Michael D. Rugg. State-related and item-related neural correlates of successful memory encoding. Nature Neuroscience 5, 1339 – 1344 (2002). Published online: 28 October 2002; doi:10.1038/nn967

Motion-Sensitive Cortex Activated By Static "Implied Motion"

Looking at static pictures of people running versus pictures of people standing still “evokes a delayed response in an area that overlaps with motionsensitive cortex (hMT+)”. Past studies have indicated a similar response for images depicting a falling cup versus a cup resting on a table.

The paper discusses the role of top-down influence from the temporal lobe as a possible cause for the response. How could this kind of brain activity be influencing our ability to recognize objects in scenes? Is this evidence of the activation of a distributed cortical representation of a moving object?

Should the field of AI be trying to figure out how to replicate a similar top-down influence in next-generation object recognition algorithms?

Abstract from the Journal of Cognitive Neuroscience is available here.

Vagus nerve stimulator for depression maybe not so great

This nytimes article points out that:

A top federal medical official overruled the unanimous opinion of his scientific staff when he decided last year to approve a pacemaker-like device to treat persistent depression, a Senate committee reported Thursday.

The device, the surgically implanted vagus nerve stimulator, had not proved effective against depression in its only clinical trial for treatment of that illness. As a result, scientists at the Food and Drug Administration repeatedly and unanimously recommended rejecting the application of its maker, Cyberonics Inc., to sell it as such a treatment, said the report, written by the staff of the Senate Finance Committee.

But Dr. Daniel G. Schultz, director of the Center for Devices and Radiological Health at the agency, kept moving the application along and eventually decided to approve it, the report said.

That approval did follow the backing of a divided F.D.A. advisory committee.


When some epilepsy patients reported that their moods had changed after receiving the devices, Cyberonics, based in Houston, implanted them in 235 depressed patients and turned the machines on in half of them. After three months, the two groups were equally depressed. The trial had failed.

Cyberonics then turned the devices on in all 235 patients and determined that 30 percent showed significant improvement after six months or more. Without a control group, however, it was impossible to determine if the device had caused the improvement.

Newsome Wants Electrode In Own Brain

Stanford Neuroscientist Bill Newsome wants to implant an electrode in his own brain to study consciousness in ways that would be difficult with volunteer human subjects.

When considered alongside the story of Kevin Warwick who had a 100-electrode array implanted in his arm in 2002 in order to study electrical signals from his hand, one must wonder: is this a starting trend?

From the article:

TR: Do you really want to do this?

BN: Well, I’ve thought about it very carefully. I’ve talked to neurosurgeons, both in the United States and outside the country where the regulatory environment is less strict, about how practical and risky it is. If the risk of serious postsurgical complications was one in one hundred, I wouldn’t do it. If it was one in one thousand, I would seriously consider doing it. To my chagrin, most surgeons estimate the risk to be somewhere in between my benchmarks.


[offtopic] Fab labs

Totally offtopic but cool.

Rehmi Post is just wrapping up his PhD. Among other things, he teaches a three month class to new students, titled “how to fabricate (almost) anything”. Students start with using CAD packages, then he takes them through fabrication of parts using machine tools, how to design circuit boards, and — literally — just about anything, up to and including MEMS, microelectromechanical machines etched out of silicon wafers using the same lithography techniques as microprocessors. “One thing we’ve learned in the course of this study is that the fabrication tools currently available all suck,” he says.

Which is why he and some other researchers are working on the Fab Lab. The goal is to build a toolkit that can be sold for under $10,000 (£6500) and that contains everything you need in order to make almost anything. “We want to take arts and crafts to a level where people can do their own prototyping, build their own radios, oscilloscopes, or computers, and do it on the cheap with full support in tools and hardware.” He’s not kidding. The Fab Lab — personal fabrication — includes a CAD workstation, a modified vinyl cutter able to carve circuit boards, a computer-controlled milling machine, an FPGA programmer, and may eventually include a 3D printer and other machine tools. One important element they’re working on is a library of electronic components, royalty-free, than the system can be used to handle various tasks. Using FPGA (field programmable gate array) chips means the system can contain sophisticated electronics — FPGAs are designed to be reconfigured at the hardware level to emulate arbitrary circuits, all the way up to an ARM processor. The Fab Lab team are trying to develop a system comprehensive enough that any one Fab Lab can be used to build copies of itself, and they’re looking at a hardware design strategy akin to the GPL (GNU General Public License) — spin offs such as Project Pengachu give a feel for how they’re thinking these tools can be used.
” — article by Charlie Stross on MIT Media lab


according to, a fab lab currently
costs about $30k; i’m assuming it’s not self-machinable yet.

Cell-chip adhesion chemistry

Berkeley researchers lay groundwork for cell version of DNA chip

This is a little off the beaten path, but I think that the Neurodudes crowd is generally interested in techniques related to neuron-to-silicon interfacing. Here’s some neat surface chemistry from Livermore Labs that facilitates binding of DNA oligos to the cell surface. Then, just like with a gene chip, you can link cells with the right (complementary) oligos to a pre-coated chip.

My first reaction to this was, Wow, another great application of the homologous base pairing machinery of nucleic acids. I’m amazed by the out-of-the-box thinking in this idea — sticking DNA to the outside of the cell. According to the article, the authors estimate that about 270,000 DNA molecules are put on the surface of each cell by their process. (Though I’m sure they’ve looked at it, one does wonder how this impacts membrane trafficking, receptor internalization processes, etc.)

Let me emphasize… This is totally cool! This allows cell-type-specific micropatterning at the level of whatever your chip printing resolution is. (Traditionally, gene chips are “spotted” using precision multi-head inkjet-like printers.) For you cell culture enthusiasts out there, you might imagine a cell culture where you have many different cell types and have full control (down to a single cell!) of where each type of cell is placed. Talk about a co-culture!

Neonatal Antidepressant Exposure has Lasting Effects

Neonatal Antidepressant Exposure has Lasting Effects on Behavior and Serotonin Circuitry [Neuropsychopharmacology]

Since we’ve had some articles on SSRIs before, I thought I’d add this one.

Here’s the central result:

In neonatal rodents, chronic administration of serotonin reuptake inhibitors (clomipramine, fluoxetine, zimeldine, LU-10-134C) as well as some other tricyclic antidepressants but not the atypical antidepressants iprindole or nomifensine during the early life period from postnatal day 8 (PN8) to PN21 results in a pattern of maladaptive behaviors that are evident long after drug discontinuation and persist into adulthood (Mirmiran et al, 1981; Hilakivi et al, 1984; Hilakivi and Hilakivi, 1987; Hansen et al, 1997; Ansorge et al, 2004). These behavioral changes, described here as the ‘neonatal antidepressant exposure syndrome (NADES)’, in rats include alterations in locomotor activity, reduced male sexual activity and competence, increased ethanol consumption, dysregulation of the hypothalamic-pituitary-adrenal axis, increased rapid eye movement (REM) sleep time and reduced latency to enter the REM sleep phase, and increased immobility in the forced swim test (Mirmiran et al, 1981; Hilakivi et al, 1984; Hilakivi and Hilakivi, 1987; Hartley et al, 1990; Hansen et al, 1997). In contrast, adults exposed to similar doses and durations of antidepressants exhibit no persistent behavioral effects after drug discontinuation, indicating that the neurobiological response to long-term antidepressant administration differs markedly between early life and adulthood.

These findings indicate that there is some early (in development) regulation of the 5HT system. Without “proper” development, the organism suffers long-lasting deficits, but if the 5HT system is exposed to modulatory SSRIs later in life, there are no long-term changes. Interesting. I wonder what developmental switches (genes, etc.) are responsible for this difference.