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Fear, Trauma and Memory: A Panel Discussion

Anne Trafton |

How accurate are our memories after a traumatic event? Does chronic stress make us more vulnerable to trauma? Will scientists one day succeed in preventing PTSD?

We invite you to join the discussion with a distinguished group of experts who will explore new lines of research and treatment strategies for stress disorders and traumatic memory. On Monday, April 7th, McGovern Institute director Bob Desimone will moderate a panel of experts and will engage the audience in a Q&A session. This event is free and open to the public, but registration is required. We hope you will join us!

 

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Fear, Trauma and Memory: A Panel Discussion

DATE: Monday April 7, 2014
TIME: 5:30 reception | 6:30 panel discussion
LOCATION: McGovern Institute for Brain Research at MIT (MIT Bldg 46-3189)
QUESTIONS? ldargus@mit.edu or 617.324.2077

 

MODERATOR

Robert DesimoneRobert Desimone is the director of the McGovern Institute and the Doris and Don Berkey Professor of Neuroscience in MIT’s Department of Brain and Cognitive Sciences. Prior to joining the McGovern Institute in 2004, he was director of the Intramural Research Program at the National Institutes of Mental Health. He is a member of the National Academy of Sciences and the American Academy of Arts and Sciences and a recipient of numerous awards, including the Troland Prize of the National Academy of Sciences.

 

 

PANELISTS

uniform photoMichael Ball is originally from Boston and is a graduate of Boston Latin Academy High School. He enlisted in the United States Marine Corps upon graduation from high school and was stationed out of Camp Lejeune, North Carolina. Ball was deployed twice to Afghanistan with the 2nd Battalion 6th Marine Regiment, and subsequently diagnosed with both post traumatic stress disorder and traumatic brain injury after receiving multiple concussions from IED blasts in southern Helmand Province. Now out of the Marine Corps for one year, Michael now volunteers to help veterans in need and spread awareness of the struggles veterans face upon separation from the military.

 

122x122-gabrieliBWJohn Gabrieli is the director of the Athinoula A. Martinos Imaging Center at the McGovern Institute. He is an Investigator at the Institute, with faculty appointments in the Department of Brain and Cognitive Sciences and the Institute for Medical Engineering at MIT. Gabrieli’s major research focus is combining brain imaging with behavioral analysis to understand the organization of memory, thought, and emotion in the human brain. A central theme of Gabrieli’s research is memory in its different forms: the short-term recall that allows us to dial a phone number, our long-term memory of events and places, and the emotional associations that often color our factual memories. These different types of memory are mediated by different brain systems, and Gabrieli seeks to tease these systems apart and understand how they interact to shape our overall sense of the past.

Prior joining MIT, Gabrieli spent 14 years at Stanford University in the Department of Psychology and Neurosciences Program. Since 1990, he has served as Visiting Professor, Department of Neurological Sciences, Rush-Presbyterian-St. Luke’s Hospital and Rush Medical College. He earned a PhD in Behavioral Neuroscience in the MIT Department of Brain and Cognitive Sciences in 1987 and BA in English from Yale University in 1978.


122x122-kigoosensBWKi Ann Goosens is a Principal Investigator at the McGovern Institute and Assistant Professor in the MIT Department of Brain and Cognitive Sciences. Goosens is currently dedicated to studying the relationship between fear, anxiety, and stress. In 2013, Goosens published new findings demonstrating that the hormone ghrelin, a stomach hormone whose production is dramatically enhanced in times of stress, makes the brain more vulnerable to traumatic events and may predispose people to post-traumatic stress disorder. Goosens hopes that a better understanding of the brain’s response to stress will lead to new therapeutic strategies for anxiety and stress disorders, depression, and other psychiatric diseases.

Prior to joining the McGovern Institute, Goosens was a postdoctoral fellow with Dr. Robert Sapolsky at Stanford University. She earned a PhD in Biopsychology from the University of Michigan, Ann Arbor, in 2002 and, prior to that, a BA with Distinction in Cognitive Science with a Concentration in Neuroscience from the University of Virginia.


Dr. Mireya Nadal-Vicens is a staff psychiatrist at Massachusetts General Hospital, where she specializes in treating individuals with stress- and trauma-related disorders. She conducts research in the Center for Anxiety and Traumatic Stress Disorder and Center for Addiction Medicine at Mass. General Hospital, and is an Instructor of Psychiatry at Harvard Medical School. Nadal-Vicens is rigorously trained in basic laboratory science in the field of brain development. Her research and training plan relates to establishing a new model for depression and social defeat, and in this work she draws from several disciplines and departments at MGH/Harvard, including psychiatry, neuroscience, pharmacology, and genetics.

Nadal-Vicens earned a BA from Harvard College, an MS in Neuroscience from Stanford University, and an MD/PhD in the Department of Neuroscience at Harvard Medical School. During her PhD thesis work, she studied the molecular signaling cascade responsible for the generation of neurons and glial cells during early brain development, working with newly discovered neural stem cells.

 

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McGovern Institute to honor neurogenetics researcher Huda Zoghbi

Anne Trafton |

The McGovern Institute for Brain Research at MIT announced today that Huda Y. Zoghbi, of Baylor College of Medicine and Texas Children’s Hospital, is the winner of the 2014 Edward M. Scolnick Prize in Neuroscience. The Prize is awarded annually by the McGovern Institute to recognize outstanding advances in the field of neuroscience.

“Huda Zoghbi has been a pioneer in the study of human genetic disease,” says Robert Desimone, director of the McGovern Institute and chair of the selection committee. “Her work has provided fundamental insights into the mechanisms of hereditary neurodegenerative and neuropsychiatric diseases, and has pointed the way to new treatments for these disorders.”

Zoghbi studied medicine in her native Lebanon and later in the US, where she specialized in pediatric neurology. Following her residency she trained as a molecular geneticist with Arthur Beaudet at Baylor College of Medicine, where she became a faculty member in 1988. She is currently an investigator with the Howard Hughes Medical Institute.

Zoghbi’s first major scientific contribution was the identification in 1993 of the gene responsible for spinocerebellar ataxia type 1 (SCA1), a progressive neurodegenerative disease with an unusual pattern of inheritance. In collaboration with Harry Orr at the University of Minnesota, Zoghbi showed that SCA1, like Huntington’s disease, is caused by a pathological expansion of a repeated three-nucleotide sequence. The more times this is repeated, the earlier the onset of disease and the more severe the symptoms. The number of repeats can increase from one generation to the next, meaning that children are often more severely affected than the parent. Zoghbi continues to study SCA1, and her recent work has focused on identifying genetic factors that slow the progression of the disease, a strategy that she hopes will also be applicable to other neurodegenerative disorders.

Zoghbi is perhaps best known for her pioneering work on Rett syndrome, a genetic neurological disease that affects young girls (males with the condition usually die in infancy). Girls born with the disease develop normally for one or two years, but then begin to show progressive loss of motor skills, speech, and other cognitive abilities.

Zoghbi first encountered children with Rett syndrome during her residency, and decided to search for its genetic cause. This was a challenging task; the disease was not widely recognized at the time and was often misdiagnosed, and family studies were difficult because the majority of cases were caused by isolated sporadic mutations. Zoghbi persisted despite these challenges, and after a 16-year search, she succeeded in identifying the Rett gene in 1999. This discovery provided a definitive genetic diagnosis for the condition, and also opened the door to a biological understanding and a search for treatment. Zoghbi demonstrated that Rett syndrome is caused by deficiency in a protein called MeCP2, which binds methylated DNA and regulates the expression of many other genes. The gene lies on the X chromosome, and in females one of the two X chromosomes is randomly inactivated in each cell; thus each patient with the Rett mutation has a different pattern of healthy and mutant cells, explaining some of the variability of Rett symptoms.

Identification of the Rett gene allowed researchers to make equivalent mutations in mouse models, which develop progressive neurological symptoms strikingly similar to those of human patients. This in turn laid the groundwork for further studies by Zoghbi and many other labs, and to the development of new therapeutic strategies that are now undergoing clinical trials.

The implications of this work extend beyond Rett syndrome (a relatively rare condition). Many Rett patients show symptoms of autism, and one hope is that understanding these symptoms may lead to new treatments that will be effective not only for people with Rett syndrome but also for other more common cases of autism. Zoghbi’s recent work has focused on identifying the cell types and brain circuits that are responsible for the autistic-like behaviors of the mouse Rett model, which may represent promising targets for future therapeutic intervention.

In addition to running her own laboratory, Zoghbi is the founding director of the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. She has received numerous awards and honors for her work, including election to both the Institute of Medicine and the National Academy of Sciences.
The McGovern Institute will award the Scolnick Prize to Dr. Zoghbi on Wednesday April 30, 2014. At 4:00 pm she will deliver a lecture entitled “A neural tipping point: MeCP2 and neuropsychiatric disorders,” to be followed by a reception, at the McGovern Institute in the Brain and Cognitive Sciences Complex, 43 Vassar Street (building 46, room 3002) in Cambridge. The event is free and open to the public.

About the Edward M. Scolnick Prize in Neuroscience:
The Scolnick Prize, awarded annually by the McGovern Institute, is named in honor of Dr. Edward M. Scolnick, who stepped down as President of Merck Research Laboratories in December 2002 after holding Merck’s top research post for 17 years. Dr. Scolnick is now a core member of the Broad Institute, where he is chief scientist at the Stanley Center for Psychiatric Research. He also serves as a member of the McGovern Institute’s governing board. The prize, which is endowed through a gift from Merck to the McGovern Institute, consists of a $100,000 award, plus an inscribed gift. Previous winners are Thomas Jessell (Columbia University), Roger Nicoll (University of California, San Francisco), Bruce McEwen (Rockefeller University), Lily and Yuh-Nung Jan (University of California, San Francisco), Jeremy Nathans (Johns Hopkins University), Michael Davis (Emory University), David Julius (University of California, San Francisco), Michael Greenberg (Harvard Medical School), Judith Rapoport (National Institute of Mental Health) and Mark Konishi (California Institute of Technology).

Broad, MIT researchers reveal structure of key CRISPR complex

Anne Trafton |

Researchers from the Broad Institute and MIT have teamed up with colleagues from the University of Tokyo to form the first high definition picture of the Cas9 complex – a key part of the CRISPR-Cas system used by scientists as a genome-editing tool to silence genes and probe the biology of cells. Their findings, which are reported this week in Cell, are expected to help researchers refine and further engineer the tool to accelerate genomic research and bring the technology closer to use in the treatment of human genetic disease.

First discovered in bacteria in 1987, CRISPRs (Clustered Regularly Interspaced Short Palindromic Repeats) have recently been harnessed as so-called genome editing tools. These tools allow researchers to home in on “typos” within the three-billion-letter sequence of the human genome, and cut out and even alter the problematic sequence. The Cas9 complex, which includes the CRISPR “cleaving” enzyme Cas9 and an RNA “guide” that leads the enzyme to its DNA target, is key to this process.

“We’ve come to view the Cas9 complex as the ultimate guided missile that we can use to target precise sites in the genome,” said co-senior author Feng Zhang, a core member of the Broad Institute, an investigator at the McGovern Institute for Brain Research, and an assistant professor at MIT. “This study provides a schematic of the entire system – it shows the missile (the Cas9 protein), the programming instructions (the guide RNA) that send it to the right location, and the target DNA. It also reveals the secret of how these pieces function together to make the whole system work.”

To deconstruct this system, Zhang approached the paper’s co-senior author Osamu Nureki at the University of Tokyo. Together, they assembled a team to work out the complicated structure.

“Cas9-based genome editing technologies are proving to be revolutionary in a wide range of life sciences, enabling many new experimental techniques, so my colleagues and I were excited to work with Feng’s lab on this important research,” said first author Hiroshi Nishimasu, an assistant professor of biophysics and biochemistry who works in Nureki’s lab at the University of Tokyo.

The two teams worked closely to reveal the structural details of the Cas9 complex and to test their functional significance. Their efforts revealed a division of labor within the Cas9 complex. The researchers determined that the Cas9 protein consists of two lobes: one lobe is involved in the recognition of the RNA and DNA elements, while the other lobe is responsible for cleaving the target DNA, causing what is known as a “double strand break” that disables the targeted gene. The team also found that key structures on Cas9 interface with the guide RNA, allowing Cas9 to organize itself around the RNA and the target DNA as it prepares to cut the strands.

Identifying the key features of the Cas9 complex should enable researchers to improve the genome-editing tool to better suit their needs.

“Up until now, it has been very difficult to rationally engineer Cas9. Now that we have this structural information, we can take a principled approach to engineering the protein to make it more effective,” said Zhang, who is also a co-founder of Editas Medicine, a company that was started last year to develop Cas9 and other genome editing technologies into a novel class of human therapeutics.

Currently, Cas9 is used in experiments to silence genes in mammalian cells – sometimes at multiple sites across the genome – and large libraries of RNA sequences have been created to guide Cas9 to genes of interest. However, the system can only target specific types of sites. Some studies have also shown that the RNA could lead Cas9 “off-target,” potentially causing unexpected problems within the cellular machinery.

The researchers plan to use this new, detailed picture of the Cas9 complex to address these concerns.

“Understanding this structure may help us engineer around the current limitations of the Cas9 complex,” said study author F. Ann Ran, a graduate student in Zhang’s lab. “In the future, it could allow us to design versions of these editing tools that are more specific to our research needs. We may even be able to alter the type of nucleic acid sequences that Cas9 can target.”

Such technological improvements will be needed if the CRISPR-Cas system is to evolve into a therapeutic tool for the treatment of genetic disease.

The study was supported by the National Institute of Mental Health (NIMH); an NIH Director’s Pioneer Award; the Japan Science and Technology Agency; the Japan Society for the Promotion of Science; the Keck, McKnight, Poitras, Merkin, Vallee, Damon Runyon, Searle Scholars, Klingenstein, and Simons Foundations; as well as Bob Metcalfe and Jane Pauley.

Other researchers who worked on the study include Patrick D. Hsu, Silvana Konermann, Soraya Shehata, Naoshi Dohmae, and Ryuichiro Ishitani.

Written by Veronica Meade-Kelly, Broad Institute

Paper cited:

Nishimasu H et al. “Crystal structure of Cas9 in complex with guide RNA and target DNA.” Cell DOI: 10.1016/j.cell.2014.02.001

About the Broad Institute of Harvard and MIT
The Eli and Edythe L. Broad Institute of Harvard and MIT was launched in 2004 to empower this generation of creative scientists to transform medicine. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.

Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to http://www.broadinstitute.org.

About the McGovern Institute for Brain Research at MIT
The McGovern Institute for Brain Research at MIT is led by a team of world-renowned neuroscientists committed to meeting two great challenges of modern science: understanding how the brain works and discovering new ways to prevent or treat brain disorders. The McGovern Institute was established in 2000 by Patrick J. McGovern and Lore Harp McGovern, who are committed to improving human welfare, communication and understanding through their support for neuroscience research. The director is Robert Desimone, formerly the head of intramural research at the National Institute of Mental Health.

Optogenetic toolkit goes multicolor

Anne Trafton |

Optogenetics is a technique that allows scientists to control neurons’ electrical activity with light by engineering them to express light-sensitive proteins. Within the past decade, it has become a very powerful tool for discovering the functions of different types of cells in the brain.

Most of these light-sensitive proteins, known as opsins, respond to light in the blue-green range. Now, a team led by MIT has discovered an opsin that is sensitive to red light, which allows researchers to independently control the activity of two populations of neurons at once, enabling much more complex studies of brain function.

“If you want to see how two different sets of cells interact, or how two populations of the same cell compete against each other, you need to be able to activate those populations independently,” says Ed Boyden, a member of the McGovern Institute for Brain Research at MIT and a senior author of the new study.

The new opsin is one of about 60 light-sensitive proteins found in a screen of 120 species of algae. The study, which appears in the Feb. 9 online edition of Nature Methods, also yielded the fastest opsin, enabling researchers to study neuron activity patterns with millisecond timescale precision.

Boyden and Gane Ka-Shu Wong, a professor of medicine and biological sciences at the University of Alberta, are the paper’s senior authors, and the lead author is MIT postdoc Nathan Klapoetke. Researchers from the Howard Hughes Medical Institute’s Janelia Farm Research Campus, the University of Pennsylvania, the University of Cologne, and the Beijing Genomics Institute also contributed to the study.

In living color

Opsins occur naturally in many algae and bacteria, which use the light-sensitive proteins to help them respond to their environment and generate energy.

To achieve optical control of neurons, scientists engineer brain cells to express the gene for an opsin, which transports ions across the cell’s membrane to alter its voltage. Depending on the opsin used, shining light on the cell either lowers the voltage and silences neuron firing, or boosts voltage and provokes the cell to generate an electrical impulse. This effect is nearly instantaneous and easily reversible.

Using this approach, researchers can selectively turn a population of cells on or off and observe what happens in the brain. However, until now, they could activate only one population at a time, because the only opsins that responded to red light also responded to blue light, so they couldn’t be paired with other opsins to control two different cell populations.

To seek additional useful opsins, the MIT researchers worked with Wong’s team at the University of Alberta, which is sequencing the transcriptomes of 1,000 plants, including some algae. (The transcriptome is similar to the genome but includes only the genes that are expressed by a cell, not the entirety of its genetic material.)

Once the team obtained genetic sequences that appeared to code for opsins, Klapoetke tested their light-responsiveness in mammalian brain tissue, working with Martha Constantine-Paton, a professor of brain and cognitive sciences and of biology, a member of the McGovern Institute for Brain Research at MIT, and also an author of the paper. The red-light-sensitive opsin, which the researchers named Chrimson, can mediate neural activity in response to light with a 735-nanometer
wavelength.

The researchers also discovered a blue-light-driven opsin that has two highly desirable traits: It operates at high speed, and it is sensitive to very dim light. This opsin, called Chronos, can be stimulated with levels of blue light that are too weak to activate Chrimson.

“You can use short pulses of dim blue light to drive the blue one, and you can use strong red light to drive Chrimson, and that allows you to do true two-color, zero-cross-talk activation in intact brain tissue,” says Boyden, who is a member of MIT’s Media Lab and an associate professor of biological engineering and brain and cognitive sciences at MIT.

Researchers had previously tried to modify naturally occurring opsins to make them respond faster and react to dimmer light, but trying to optimize one feature often made other features worse.

“It was apparent that when trying to engineer traits like color, light sensitivity, and kinetics, there are always tradeoffs,” Klapoetke says. “We’re very lucky that something natural actually was more than several times faster and also five or six times more light-sensitive than anything else.”

Selective control

These new opsins lend themselves to several types of studies that were not possible before, Boyden says. For one, scientists could not only manipulate activity of a cell population of interest, but also control upstream cells that influence the target population by secreting neurotransmitters.

Pairing Chrimson and Chronos could also allow scientists to study the functions of different types of cells in the same microcircuit within the brain. Such cells are usually located very close together, but with the new opsins they can be controlled independently with two different colors of light.

“I think the tools described in this excellent paper represent a major advance for both basic and translational neuroscience,” says Botond Roska, a senior group leader at the Friedrich Miescher Institute for Biomedical Research in Switzerland, who was not part of the research team. “Optogenetic tools that are shifted towards the infrared range, such as Chrimson described in this paper, are much better than the more blue-shifted variants since these are less toxic, activate less the pupillary reflex, and activate less the remaining photoreceptors of patients.”

Most optogenetic studies thus far have been done in mice, but Chrimson could be used for optogenetic studies of fruit flies, a commonly used experimental organism. Researchers have had trouble using blue-light-sensitive opsins in fruit flies because the light can get into the flies’ eyes and startle them, interfering with the behavior being studied.

Vivek Jayaraman, a research group leader at Janelia Farms and an author of the paper, was able to show that this startle response does not occur when red light is used to stimulate Chrimson in fruit flies.

Because red light is less damaging to tissue than blue light, Chrimson also holds potential for eventual therapeutic use in humans, Boyden says. Animal studies with other opsins have shown promise in helping to restore vision after the loss of photoreceptor cells in the retina.

The researchers are now trying to modify Chrimson to respond to light in the infrared range. They are also working on making both Chrimson and Chronos faster and more light sensitive.

MIT’s portion of the project was funded by the National Institutes of Health, the MIT Media Lab, the National Science Foundation, the Wallace H. Coulter Foundation, the Alfred P. Sloan Foundation, a NARSAD Young Investigator Grant, the Human Frontiers Science Program, an NYSCF Robertson Neuroscience Investigator Award, the IET A.F. Harvey Prize, Janet and Sheldon Razin ’59, and the Skolkovo Institute of Science and Technology.

2014 Phillip A. Sharp Lecture in Neural Circuits

Anne Trafton |

In the 2014 Sharp Lecture, May-Britt Moser of the Norwegian University of Science and Technology described her work on “grid cells,” which she co-discovered with husband Edvard Moser in 2005. The activity of these cells suggests that the brain maps 2D space onto a grid from which the animal’s location can be computed.

Expanding our view of vision

Anne Trafton |

Every time you open your eyes, visual information flows into your brain, which interprets what you’re seeing. Now, for the first time, MIT neuroscientists have noninvasively mapped this flow of information in the human brain with unique accuracy, using a novel brain-scanning technique.

This technique, which combines two existing technologies, allows researchers to identify precisely both the location and timing of human brain activity. Using this new approach, the MIT researchers scanned individuals’ brains as they looked at different images and were able to pinpoint, to the millisecond, when the brain recognizes and categorizes an object, and where these processes occur.

“This method gives you a visualization of ‘when’ and ‘where’ at the same time. It’s a window into processes happening at the millisecond and millimeter scale,” says Aude Oliva, a principal research scientist in MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL).

Oliva is the senior author of a paper describing the findings in the Jan. 26 issue of Nature Neuroscience. Lead author of the paper is CSAIL postdoc Radoslaw Cichy. Dimitrios Pantazis, a research scientist at MIT’s McGovern Institute for Brain Research, is also an author of the paper.

When and where

Until now, scientists have been able to observe the location or timing of human brain activity at high resolution, but not both, because different imaging techniques are not easily combined. The most commonly used type of brain scan, functional magnetic resonance imaging (fMRI), measures changes in blood flow, revealing which parts of the brain are involved in a particular task. However, it works too slowly to keep up with the brain’s millisecond-by-millisecond dynamics.

Another imaging technique, known as magnetoencephalography (MEG), uses an array of hundreds of sensors encircling the head to measure magnetic fields produced by neuronal activity in the brain. These sensors offer a dynamic portrait of brain activity over time, down to the millisecond, but do not tell the precise location of the signals.

To combine the time and location information generated by these two scanners, the researchers used a computational technique called representational similarity analysis, which relies on the fact that two similar objects (such as two human faces) that provoke similar signals in fMRI will also produce similar signals in MEG. This method has been used before to link fMRI with recordings of neuronal electrical activity in monkeys, but the MIT researchers are the first to use it to link fMRI and MEG data from human subjects.

In the study, the researchers scanned 16 human volunteers as they looked at a series of 92 images, including faces, animals, and natural and manmade objects. Each image was shown for half a second.

“We wanted to measure how visual information flows through the brain. It’s just pure automatic machinery that starts every time you open your eyes, and it’s incredibly fast,” Cichy says. “This is a very complex process, and we have not yet looked at higher cognitive processes that come later, such as recalling thoughts and memories when you are watching objects.”

Each subject underwent the test multiple times — twice in an fMRI scanner and twice in an MEG scanner — giving the researchers a huge set of data on the timing and location of brain activity. All of the scanning was done at the Athinoula A. Martinos Imaging Center at the McGovern Institute.

Millisecond by millisecond

By analyzing this data, the researchers produced a timeline of the brain’s object-recognition pathway that is very similar to results previously obtained by recording electrical signals in the visual cortex of monkeys, a technique that is extremely accurate but too invasive to use in humans.

About 50 milliseconds after subjects saw an image, visual information entered a part of the brain called the primary visual cortex, or V1, which recognizes basic elements of a shape, such as whether it is round or elongated. The information then flowed to the inferotemporal cortex, where the brain identified the object as early as 120 milliseconds. Within 160 milliseconds, all objects had been classified into categories such as plant or animal.

The MIT team’s strategy “provides a rich new source of evidence on this highly dynamic process,” says Nikolaus Kriegeskorte, a principal investigator in cognition and brain sciences at Cambridge University.

“The combination of MEG and fMRI in humans is no surrogate for invasive animal studies with techniques that simultaneously have high spatial and temporal precision, but Cichy et al. come closer to characterizing the dynamic emergence of representational geometries across stages of processing in humans than any previous work. The approach will be useful for future studies elucidating other perceptual and cognitive processes,” says Kriegeskorte, who was not part of the research team.

The MIT researchers are now using representational similarity analysis to study the accuracy of computer models of vision by comparing brain scan data with the models’ predictions of how vision works.

Using this approach, scientists should also be able to study how the human brain analyzes other types of information such as motor, verbal, or sensory signals, the researchers say. It could also shed light on processes that underlie conditions such as memory disorders or dyslexia, and could benefit patients suffering from paralysis or neurodegenerative diseases.

“This is the first time that MEG and fMRI have been connected in this way, giving us a unique perspective,” Pantazis says. “We now have the tools to precisely map brain function both in space and time, opening up tremendous possibilities to study the human brain.”

The research was funded by the National Eye Institute, the National Science Foundation, and a Feodor Lynen Research Fellowship from the Humboldt Foundation.

SAPAP-4

Anne Trafton |

Neurons in the mouse cerebellum, expressing the synaptic protein SAPAP-4. Image: Louis Tee and Guoping Feng

2014 Phillip A. Sharp Lecture in Neural Circuits

Anne Trafton |

SPEAKER: Dr. May-Britt Moser
ORGANIZATION: Kavli Institute for Systems Neuroscience
DATE + TIME: Wednesday February 5, 2014 at 4pm
LOCATION: MIT Bldg 46-3002 (Singleton Auditorium)

ABSTRACT: The medial entorhinal cortex (MEC) is part of the brain’s circuit for dynamic representation of self-location. The metric of this representation is provided by grid cells, cells with spatial firing fields that tile environments in a periodic hexagonal pattern. I will begin my lecture by discussing how grid cells are organized within the MEC. Based on recordings from large numbers of grid cells in individual rats, I will show that grid cells cluster into a small number of layer-spanning anatomically-overlapping functionally independent modules with distinct scale and orientation – a property that may be advantage to high-capacity memory in output areas such as the hippocampus. I will further discuss how inputs from grid cells and other functional cell types determine properties of place cells in the hippocampus. Using a combination of electrophysiological and optogenetic techniques, we find that the hippocampus receives input from a variety of sources, including border cells and head direction cells in the MEC, odour-responsive cells in the lateral entorhinal cortex, and, via the nucleus reuniens, decision-correlated cells in the medial prefrontal cortex. Collectively these inputs may be enable memory in ensembles of place cells in the hippocampus.

A Personal Message from Lore Harp McGovern

Anne Trafton |

Charles M. Vest’s death came much too early. I miss this man terribly, his kindness, his intelligence, his fairness and most of all his simple humanity. Chuck was President of MIT when we started our discussion about the possibility of the McGovern Institute to be located at MIT. He was enthusiastic, if not ecstatic, but exercised reserve and a deep felt appreciation for what this would mean for neuroscience at MIT.

Our lengthy discussions and negotiations, some not so easy, were always fair with a win-win in mind, and his humorous use of narratives was a tactic to try and sway you without you noticing. I remember the time we met so I could listen to his rationale about postponing the start of building the MIBR. Of course we were opposed to that, and so I was invited by Chuck to a private lunch with the model of the building prominently displayed in view of our table. As in chess, where you try to corner the queen, Chuck suggested that we trade places, thereby putting the model in a less favorable light, all in the hope he could meet his objective. Oh Chuck! We started and finished pretty much on schedule. So many memories, bear hugs and laughter. I remember an MIT dinner where attendees were leaving, but you and I kept talking, the room cleared out, tables were folded up, the crew swept the floor around us sitting on our chairs, ignoring all. The topic of discussion still centered around the building. And then there always will be the story of French fries at Marché in Menlo Park! Chuck was passing the baton and visited many people across the country to say thank you. I had the pleasure to have dinner with him. Chuck was a runner and in great shape because he was mindful of what he ate; however, both of us ordered that occasional steak and unbeknown to us it was accompanied by two enormous pointed parchment bags in a gracious holder filled with (alas, delicious) French fries! We first looked at them in disdain, but one after the other they disappeared until they were gone. We laughed and tried to excuse away the consumption of all those French fries, and with a huge smile on your face “French fries” became your greeting to the bewilderment of those around us. You also shared private dreams post presidency about being interested in an ambassadorship, but that that would be not be feasible for different reasons. I wish we could have many more of our conversations, but instead I wish you goodbye with one last bear hug!

Be well in the place souls go to rest, my friend, and know that you were respected for all the right reasons, but loved by many and by me because you were very simply, Chuck!

Viral Core Image Gallery

Anne Trafton |

To view the viral core image gallery, please click on one of the thumbnail images below.