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Breaking News from Society for Neuroscience 2012

For release: Wednesday, October 17, 2012

Hundreds of NIH-funded studies are being presented at the 2012 Society for Neuroscience annual meeting, taking place in New Orleans, Oct. 13-17.

This page highlights some of the studies and events supported by the National Institute of Neurological Disorders and Stroke, and is being updated daily throughout the meeting.

Wednesday, October 17

Signs of Lung Control and Air Breathing Found in an Ancient, Lungless Animal
     M. Hoffman, B.E. Taylor, M.B. Harris
     University of Alaska Fairbanks

Hoffman et al. have found that lampreys – which are gilled, fish-like animals – appear to have a brain respiratory control center similar to that found in air-breathing animals. Their work has implications for how air breathing and lung control evolved, and for understanding the brain circuitry that generates respiratory rhythms. The origin of rhythmic air breathing is unknown. Fish typically breathe by obtaining oxygen from water as it flows over their gills. One exception is the lungfish, which is considered a critical evolutionary link between aquatic animals and air-breathing vertebrates. But the work by Hoffman et al. suggests that the rudiments of air breathing evolved long before the lungfish did. The researchers show that lampreys, which are among the most ancient vertebrates, have a cough-like behavior that could represent a precursor of air breathing. This cough is also driven by a group of rhythmically firing neurons – or pattern generator– in the brainstem that is distinct from the pattern generator involved in gill respiration.

SfN Abstract Title & Presentation #: Lung control from lungless vertebrates – 796.04

Nanosymposium Lecture
*Omega-3 Fatty Acids May Counteract Problems in the Brain Associated with Obesity
     R. Agrawal, F. Gomez-Pinilla
     University of California Los Angeles

Obesity is a growing problem in the United States. Metabolic syndrome (MetS) is a collection of obesity-related risk factors that increase the chances of coronary artery disease, stroke, and type 2 diabetes. Traditionally MetS has been thought to cause metabolic problems in the body. Here researchers demonstrate that MetS may cause metabolic problems in the brain. MetS was induced by feeding mice high fructose and varying amounts of docosahexaenoic acid (DHA), a naturally occurring omega-3 fatty acid known to reduce some MetS risk factors. Mice fed high fructose and low DHA had memory deficits. Biochemical experiments suggested that these deficits may be caused by changes in brain metabolism and that increased levels of DHA may counteract the changes. These initial studies suggest that MetS causes problems in the brain and that certain omega 3 fatty acids may reduce them.

SfN Abstract Title & Presentation #: Metabolic syndrome in the brain: How the balance between sugars and omega-3 fatty acid determines cognitive plasticity – 726.13

Scientists Discover How Eye Synapses May Adjust to Light and Shadows
     N. W. Oesch, J.S. Diamond
     National Institute of Neurological Diseases and Stroke, Bethesda, MD

Every fraction of a second the eye adjusts to give clear pictures of the world. Oesch et al. studies the circuitry controlling many of these adjustments which is found in the retina, the tissue in the eye that converts light in nerve signals sent to the brain. Recently Oesch et al. showed that certain neurons in the retina, called rod bipolar cells (RBCs), may compute light and shadows by changing the way they release the neurotransmitter glutamate at synapses. In response, some neighboring cells, such as A17 amarcine cells may release another neurotransmitter, called GABA, back onto RBCs. Previous studies have shown GABA release from A17 amarcine cells onto RBCs may in turn modulate the way RBCs release glutamate. In this presentation the researchers show that this feedback loop made between RBCs and A17 amacrine cells may fine tune, or adjust, the way RBCs compute changes in light and shadows that the eye constantly detects.

Feedback inhibition extends the dynamic range of luminance and contrast – 879.02


Tuesday, October 16

Stimulating the Brain’s Visual Cortex Might Restore Sight
     X. Pei, P. Sun, I.M. Schepers, M.S. Beauchamp, D. Yoshor
     Baylor College of Medicine, Houston, TX; University of Texas Health Sciences Center at Houston

Pei et al. have conducted a pilot study that lays the foundation for brain implants that could restore vision to blind people. The researchers studied three sighted individuals who had electrodes implanted in their brains as part of treatment for epilepsy. By showing the patients a series of images and recording from the electrodes, the researchers created a map of receptive fields in the visual cortex – the parts of the visual field that a cell or group of cells in the cortex can see. Delivering stimulation through the same electrodes caused the patients to see spots of light called phosphenes. Next, the researchers used the receptive field maps to create a test image that they theorized would match the phosphenes that patients would see during stimulation at specific electrodes. In repeated trials, the patients received the stimulation, and then were shown the test image and a copy of it rotated by 90 degrees, in random order. When asked to pick the image that best matched the phosphene, they chose the original test image in 88 percent of trials. This shows that it is possible to predict visual perceptions elicited by stimulation of the visual cortex.

SfN Abstract Title & Presentation #: Creating visual percepts with electrical stimulation of human visual cortex: Comparison with receptive fields mapped with local field potentials – 570.21

Learn How Scientists are Tracing Our Brains’ Connections
     V. Wedeen, K Ugurbil, J.Johansen-Berg, D.C. Van Essen
     Massachusetts General Hospital, Charleston, MA; University of Minnesota, Minneapolis;
     Oxford University, UK; Washington University School of Medicine, St. Louis, MO

Never-before-seen high resolution images of the human brain’s wiring were unveiled earlier this year – the first fruit of a $40 million initiative to map the brain’s connections, now in its second year. This fall, for the first time, Human Connectome Project data is being made freely available to the neuroscience community on the web. The multi-site study, by two collaborating research consortia, is paving the way toward a detailed understanding of how our brain circuitry changes as we age – and what goes awry in brain disorders. Using customized scanners, researchers are capturing the brain’s anatomical wiring as well as its activity in 1200 healthy adults – twin pairs and their siblings from 300 families. Optimized diffusion MRI technology for imaging the brain’s long distance connections is revealing a strikingly elegant grid-like organization at multiple levels.

SfN Abstract Title & Presentation #: The Human Connectome Project – 509

Smoking May be a Potential Biomarker for Chronic Pain
     S. Torbey, A. Mansour, K. Herrmann, M. Baliki, T. Schnitzer, A. Apkarian
     Northwestern University, Chicago, IL

Chronic pain is a debilitating disorder affecting millions worldwide. Early identification of acute pain patients susceptible to chronic pain may improve diagnoses and treatments. Here researchers searched for chronic pain biomarkers by studying 62 lower back pain patients who had little history of lower back pain. The patients completed pain and life-style questionnaires during six hospital visits over one year. Twenty six patients had persistent pain whereas the remaining 36 patients recovered. Interestingly, smokers were more likely to have persistent pain and smoking was the strongest predictor that a patient would have persistent pain after the first visit, even stronger than pain levels. These preliminary results suggest smoking is a chronic pain biomarker. In the future, more conclusive studies will be needed before doctors can use smoking status to determine whether an acute pain patient is susceptible to chronic pain.

SfN Abstract Title & Presentation #: Strong association between smoking and transition from acute to chronic back pain – 675.18


Monday, October 15

Nanosymposium Lecture
Soluble Forms of Amyloid-β May Cause Dementia in Alzheimer’s Disease
     D.R. Borchelt, T. Melnikova, S. Fromholt, H. Kim, D. Lee, G. Xu, K. Felsenstein, A. Savonenko
     University of Florida, Gainesville; Johns Hopkins University School of Medicine, Baltimore, MD

Insoluble plaques made primarily of amyloid-β peptides (Aβ42) are a hallmark of Alzheimer’s disease (AD) brain pathology. Traditionally it has been thought that Aβ42 found in plaques or in protein complexes may cause dementia. Here researchers tested this idea on transgenic mice in which Aβ42 expression was controlled by a drug called doxycycline. Normally the mice express high levels of Aβ42 and develop problems with learning and memory a year after birth. Feeding these one-year old mice doxycycline reduced Aβ42 expression and improved learning and memory to levels seen in wild type mice that do not have the transgene. Interestingly, mice fed doxycycline had the same levels of insoluble Aβ42 deposits and Aβ42 complexes as mice fed normal diets whereas doxycycline rapidly decreased soluble forms of Aβ42, suggesting the soluble forms may cause dementia. These other forms of Aβ42 may provide researchers with more specific targets for treating AD.

SfN Abstract Title & Presentation #: Rapid reversal of cognitive impairment by suppression of mutant APP expression in a regulated transgenic model of Alzheimer-amyloidosis – 416.05

Reflex Control Might Improve Walking after Some Spinal Injuries
     A. Thompson, F. Pomerantz, J. Wolpaw
     New York State Department of Health, Albany; Columbia University, New York, NY; State
     University of New York at Albany

Spinal cord injuries (SCI) not only damage the nerve fibers needed for conscious movement but those needed for reflex control, leading to exaggerated reflexes that can further interfere with mobility. Thompson et al. theorized that patients with incomplete SCI (partial severing of the spinal cord) might gain mobility if they could learn to suppress their spinal reflexes. In a small trial, they trained such patients to suppress a spinal “H-reflex,” a reflex elicited by electrical stimulation rather than by a tendon stretch. During training, the patients received weak electrical stimulation to their more impaired leg while standing, and were encouraged to suppress the resulting H-reflex. After 30 such training sessions given over 10 weeks, six of nine patients achieved a smaller H-reflex, and their walking became faster and more symmetrical. These changes were not observed in four patients who received the electrical stimulation without any feedback about their H-reflex. The researchers conclude that “H-reflex down-conditioning” could be used to complement more traditional SCI rehabilitation methods.

SfN Abstract Title & Presentation #: Operant down-conditioning of the soleus H-reflex can improve gait in people with spasticity due to chronic incomplete spinal cord injury – 475.18

Nanosymposium Lecture
Brain Stimulation Methods May Improve Recovery from Stroke
     L.G. Cohen
     National Institute of Neurological Disorders and Stroke, Bethesda, MD

After a stroke, about one third of patients are disabled long-term, most often with mobility problems. Exercise and physical therapy have long been used to help such patients recover. Recent studies have shown that these interventions help re-organize the brain, with uninjured brain tissue near the damaged area forming new connections to deeper brain regions. Cohen and other researchers are investigating the use of brain stimulation methods to enhance these compensatory changes. For example, in a technique called transcranial direct current stimulation (tDCS), electrodes are placed over the scalp and used to deliver electrical currents to the brain. In pilot studies, applying tDCS near the stroke lesion has helped patients achieve small improvements in mobility. Cohen will present the latest research on using tDCS and other brain stimulation methods to improve recovery after a stroke.

SfN Abstract Title & Presentation #: Modulation of neural structures underlying motor function after stroke – 407.05

Sunday, October 14

Brain Scans May Predict Susceptibility for Chronic Back Pain
     A. Mansour, M. Baliki, L. Huang, S. Torbey, K. Herrmann, T. Schnitzer, A. Apkarian
     Northwestern University, Chicago, IL

Chronic lower back pain can be disabling and costly for patients. Early detection of acute patients susceptible to chronic pain could help doctors reduce a patient’s burden. Recent studies suggest that chronic pain is associated with changes in the brain. Here researchers used functional magnetic resonance imaging (fMRI) to study white matter density in the brains of acute lower back pain patients. The patients’ brains were scanned four times over one year. Some patients recovered and others had persistent pain throughout the year. Persistent pain patients had lower white matter density in certain brain regions whereas recovered patients had the same density as control patients who had no pain. More importantly, lower white matter density measured in the first scan was a strong predictor of whether a patient would have persistent pain. The results suggest that measuring white matter density may help doctors determine early whether pain patients are susceptible to chronic lower back pain, if not other forms of pain.

SfN Abstract Title & Presentation #:
Brain white matter abnormalities predicting transition from acute to chronic back pain - 181.18

Nanosymposium Lecture
A Boost to Protein-Handling Systems Might Help in Huntington’s
     A.C. Daub, H. Zahed, I.H. Kratter, S. Finkbeiner
     Gladstone Institutes, San Francisco, CA; University of San Francisco, CA

The mutant gene behind Huntington’s disease –named huntingtin (Htt) – triggers a relentless attack on the brain, leading to motor impairment, cognitive decline and ultimately death. Recent studies have shown that the mutant Htt protein accumulates inside neurons and appears to have a variety of toxic effects. Researchers theorize that boosting a cell’s ability to repair or dispose of abnormal proteins might reduce this toxicity. To test the theory, Daub et al. introduced mutant Htt into cultured neurons, and used an automated microscopy system to monitor the cells’ health over time. Next, they gave some of the neurons extra copies of genes involved in a protein repair mechanism. They also tried adding a tag to the mutant Htt protein that would target it for destruction. Both of these interventions improved the survival of the cultured neurons, suggesting that drugs targeting multiple aspects of cellular protein handling might be beneficial against Huntington’s disease.

SfN Abstract Title & Presentation #: Improving protein homeostasis capacity in neurons counteracts misfolded protein stress caused by mutant huntingtin – 221.12

Last Modified December 24, 2013