The annual McGovern Institute symposium took place on May 8, 2013 and featured nine talks on the subject of motor control and the motor cortex. In this video, Neville Hogan of MIT presents his talk entitled, “Modular dynamics in motor control and neuro-rehabilitation.”
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Emile Bruneau: Tweaking the Empathy Gap
Emile Bruneau, a postdoctoral associate in Rebecca Saxe’s lab at the McGovern Institute, is interested in the psychology of human conflict. He is working with Saxe to figure out why empathy — the ability to feel compassion for another person’s suffering — often fails between members of opposing conflict groups. Bruneau is also trying to locate patterns of brain activity that correlate with empathy, in hopes of eventually using such measures to determine how well people respond to reconciliation programs aimed at boosting empathy between groups in conflict.
Read more about Emile Bruneau’s work in the New York Times magazine.
Ann Graybiel Meets the President of the United States
President Barack Obama greets the 2012 U.S. Kavli Prize Laureates in the Oval Office, March 28, 2013.
Obama hosts Dresselhaus, Graybiel and Luu in Oval Office
President Barack Obama met Thursday, March 28, in the Oval Office with the six U.S. recipients of the 2012 Kavli Prizes — including MIT’s Mildred S. Dresselhaus, Ann M. Graybiel and Jane X. Luu. Obama and his science and technology advisor, John P. Holdren, received the scientists to recognize their landmark contributions in nanoscience, neuroscience and astrophysics, respectively. [watch video]
“American scientists, engineers and innovators strengthen our nation every day and in countless ways, but the all-stars honored by the Kavli Foundation deserve special praise for the scale of their advances in some of the most important and exciting research disciplines today,” said Holdren, who also serves as director of the White House Office of Science and Technology Policy. “I am grateful not only for their profound accomplishments, but for the inspiration they are providing to a new generation of doers, makers and discoverers.”
The researchers received their Kavli Prizes for making fundamental contributions to our understanding of the outer solar system; of the differences in material properties at nano- and larger scales; and of how the brain receives and responds to sensations such as sight, sound and touch.
The 2012 Kavli Prize in Astrophysics was awarded to Luu, David C. Jewitt of the University of California at Los Angeles, and Michael E. Brown of the California Institute of Technology for discovering and characterizing the Kuiper Belt and its largest members, work that led to a major advance in the understanding of the history of our planetary system. The Kuiper Belt lies beyond the orbit of Neptune and is a disk of more than 70,000 small bodies made of rock and ice, and orbiting the sun. Jewitt and Luu discovered the Kuiper Belt, and Brown discovered and characterized many of its largest members.
The 2012 Kavli Prize in Nanoscience was awarded to Dresselhaus for her work explaining why the properties of materials structured at the nanoscale can vary so much from those of the same materials at larger dimensions. Her early work provided the foundation for later discoveries concerning the famous C60 buckyball, carbon nanotubes and graphene. Dresselhaus received the Kavli Prize for her research into uniform oscillations of elastic arrangements of atoms or molecules called phonons; phonon-electron interactions; and heat conductivity in nanostructures.
The 2012 Kavli Prize in Neuroscience was awarded to Graybiel, Cornelia Isabella Bargmann of Rockefeller University, and Winfried Denk of the Max Planck Institute for Medical Research, who have pioneered the study of how sensory signals pass from the point of sensation — whether the eye, the foot or the nose — to the brain, and how decisions are made to respond. Each working on different parts of the brain, and using different techniques and models, they have combined precise neuroanatomy with sophisticated functional studies to gain understanding of their chosen systems.
MIT researchers join Obama for brain announcement
Four MIT neuroscientists were among those invited to the White House on Tuesday, April 2, when President Barack Obama announced a new initiative to understand the human brain.
Professors Ed Boyden, Emery Brown, Robert Desimone and Sebastian Seung were among a group of leading researchers who joined Obama for the announcement, along with Francis Collins, director of the National Institutes of Health, and representatives of federal and private funders of neuroscience research.
In unveiling the BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative, Obama highlighted brain research as one of his administration’s “grand challenges” — ambitious yet achievable goals that demand new innovations and breakthroughs in science and technology.
A key goal of the BRAIN Initiative will be to accelerate the development of new technologies to visualize brain activity and to understand how this activity is linked to behavior and to brain disorders.
“There is this enormous mystery waiting to be unlocked,” Obama said, “and the BRAIN Initiative will change that by giving scientists the tools they need to get a dynamic picture of the brain in action and better understand how we think and how we learn and how we remember. And that knowledge could be — will be — transformative.”
To jump-start the initiative, the NIH, the Defense Advanced Research Projects Agency, and the National Science Foundation will invest some $100 million in research support beginning in the next fiscal year. Planning will be overseen by a working group co-chaired by Cornelia Bargmann PhD ’87, now at Rockefeller University, and William Newsome of Stanford University. Brown, an MIT professor of computational neuroscience and of health sciences and technology, will serve as a member of the working group.
Boyden, the Benesse Career Development Associate Professor of Research in Engineering, has pioneered the development of new technologies for studying brain activity. Desimone, the Doris and Don Berkey Professor of Neuroscience, is director of MIT’s McGovern Institute for Brain Research, which conducts research in many areas relevant to the new initiative. Seung, a professor of computational neuroscience and physics, is a leader in the field of “connectomics,” the effort to describe the wiring diagram of the brain.
2013 Scolnick Prize Lecture: Thomas Jessell
Dr. Thomas Jessell of Columbia University is the winner of the 2013 Scolnick Prize in Neuroscience for his pioneering work on synaptic plasticity, the process by which the brain’s connections are modified in response to experience.
On April 1, 2013, he delivered the Scolnick Prize lecture, entitled “Sifting Circuits for Motor Control.”
Brain Scan Cover Image: Winter 2013
The cover of the Winter 2013 issue of Brain Scan features an artist’s representation of a new genome editing technique developed by Feng Zhang. The method allows researchers to disrupt or replace genes at will.
2013 Sharp Lecture in Neural Circuits: Karel Svoboda
On March 14, 2013, Dr. Karel Svoboda of HHMI delivered the second annual Sharp Lecture in Neuroscience. Dr. Svoboda’s lab is working on the structure, function and plasticity of neocortical circuits.
Martha Constantine-Paton to receive top honors from Tufts University
Martha Constantine-Paton will receive the Dean’s Medal from Tufts University’s School of Arts and Sciences for her “exceptional contributions to the field of developmental neuroscience.” Constantine-Paton, a Tufts alumna, refers to her time at the university as a “turning point” in her life and credits the school for giving her the self-confidence she needed to pursue a career in science. The Dean’s Medal is the highest honor available at each school at Tufts, reserved only “for those select individuals who have made outstanding contributions to the university and to the greater community.”
Constantine-Paton will be awarded the Dean’s Medal on March 25, 2013.
Breaking down the Parkinson’s pathway
The key hallmark of Parkinson’s disease is a slowdown of movement caused by a cutoff in the supply of dopamine to the brain region responsible for coordinating movement. While scientists have understood this general process for many years, the exact details of how this happens are still murky.
“We know the neurotransmitter, we know roughly the pathways in the brain that are being affected, but when you come right down to it and ask what exactly is the sequence of events that occurs in the brain, that gets a little tougher,” says Ann Graybiel, an MIT Institute Professor and member of MIT’s McGovern Institute for Brain Research.
A new study from Graybiel’s lab offers insight into some of the precise impairments caused by the loss of dopamine in brain cells affected by Parkinson’s disease. The findings, which appear in the March 12 online edition of the Journal of Neuroscience, could help researchers not only better understand the disease, but also develop more targeted treatments.
Lead author of the paper is Ledia Hernandez, a former MIT postdoc. Other authors are McGovern Institute research scientists Yasuo Kubota and Dan Hu, former MIT graduate student Mark Howe and graduate student Nuné Lemaire.
Cutting off dopamine
The neurons responsible for coordinating movement are located in a part of the brain called the striatum, which receives information from two major sources — the neocortex and a tiny region known as the substantia nigra. The cortex relays sensory information as well as plans for future action, while the substantia nigra sends dopamine that helps to coordinate all of the cortical input.
“This dopamine somehow modulates the circuit interactions in such a way that we don’t move too much, we don’t move too little, we don’t move too fast or too slow, and we don’t get overly repetitive in the movements that we make. We’re just right,” Graybiel says.
Parkinson’s disease develops when the neurons connecting the substantia nigra to the striatum die, cutting off a critical dopamine source; in a process that is not entirely understood, too little dopamine translates to difficulty initiating movement. Most Parkinson’s patients receive L-dopa, which can substitute for the lost dopamine. However, the effects usually wear off after five to 10 years, and complications appear.
To study exactly how dopamine loss affects the striatum, the researchers disabled dopamine-releasing cells on one side of the striatum, in rats. This mimics what usually happens in the early stages of Parkinson’s disease, when dopamine input is cut off on only one side of the brain.
As the rats learned to run a T-shaped maze, the researchers recorded electrical activity in many individual neurons. The rats were rewarded for correctly choosing to run left or right as they approached the T, depending on the cue that they heard.
The researchers focused on two types of neurons: projection neurons, which send messages from the striatum to the neocortex to initiate or halt movement, and fast-spiking interneurons, which enable local communication within the striatum. Among the projection neurons, the researchers identified two subtypes — those that were active just before the rats began running, and those that were active during the run.
In the dopamine-depleted striatum, the researchers found, to their surprise, that the projection neurons still developed relatively normal activity patterns. However, they became even more active during the time when they were usually active (before or during the run). These hyper-drive effects were related to whether the rats had learned the maze task or not.
The interneurons, however, never developed the firing patterns seen in normal interneurons during learning, even after the rats had learned to run the maze. The local circuits were disabled.
Restoring neuron function
When the researchers then treated the rats with L-dopa, the drug restored normal activity in the projection neurons, but did not bring back normal activity in the interneurons. A possible reason for that is that those cells become disconnected by the loss of dopamine, so even when L-dopa is given, they can no longer shape the local circuits to respond to it.
This is the first study to show that the effects of dopamine loss depend not only on the type of neuron, but also on the phase of task behavior and how well the task has been learned, according to the researchers. To glean even more detail, Graybiel’s lab is now working on measuring dopamine levels in different parts of the brain as the dopamine-depleted rats learn new behaviors.
The lab is also seeking ways to restore function to the striatal interneurons that don’t respond to L-dopa treatment. The findings underscore the need for therapies that target specific deficiencies, says Joshua Goldberg, a senior lecturer in medical neurobiology at the Hebrew University of Jerusalem.
The new study “refines our appreciation of the complexity of [Parkinson’s],” says Goldberg, who was not part of the research team. “Graybiel’s team drives home the message that dopamine depletion, and dopamine replacement therapy, do not affect brain dynamics or behavior in a uniform fashion. Instead, their effect is highly context-dependent and differentially affects various populations of neurons.”
The research was funded by the National Institutes of Health/National Institute of Neurological Disorders and Stroke, the National Parkinson Foundation, the Stanley H. and Sheila G. Sydney Fund, a Parkinson’s Disease Foundation Fellowship and a Fulbright Fellowship.