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Monitoring Dopamine Release During Reward Learning
Monitoring Dopamine Release During Reward Learning Mon, 19 Dec 2011 13:28:58 -0500 05/07/2009 3:30 PM 46"3002Paul Phillips, University of Washington, Seattle Description: In the process of learning, we "sometimes make more deliberative choices, and sometimes make more visceral ones," says Paul Phillips. These are "semantic terms we intuitively know," and scientists have become well"versed in creating tasks for animals and humans that demonstrate how these different kinds of learning (analytical" reflective vs. impulsive "reflexive) play out. Phillips has been trying to track dopamine release (a neurotransmitter linked to learning) in such divergent learning processes. The model"based learning system pairs a stimulus with a reward, and after training, a subject creates a "model representation of the world" that allows it to predict the appearance of the reward after the stimulus. In contrast, the model"free system of learning "uses a one dimensional value that gets updated" as the subject accumulates experience and begins to weigh the difference between expectation and the reward that's actually delivered. One of Phillips' studies involved implanting electrodes for measuring dopamine release in the striatum of rats participating in different types of learning tasks. Phillips work shows time"dependent changes in the release of dopamine during classic conditioning tasks. At first the dopamine spikes only after the reward, but over time, the animal learns it will receive the reward after the stimulus (a light cue), and soon, the cue alone elicits the dopamine response. Phillips has also found that two distinct parts of the striatum register increased dopamine at different points in the training. "This is quite interesting in terms of thinking about what these brain regions have been implicated in, and specifically the idea of habits in the dorsal striatum." The results of some research suggest that during these learning processes, all the dopamine neurons should be firing. But Phillips says this doesn't explain why "we're getting signals in (one) part of the brain but not in the other." Phillips speculates that dopamine's "arch nemesis acetylcholine" might be inhibiting dopamine release in certain parts of the striatum during specific phases of reinforcement learning. Phillips has also been working with selectively bred lines of rats, which seem to exhibit behaviors, and dopamine release patterns, suggestive of two distinct learning strategies. He concludes that "associations between stimuli and rewards can be learned through multiple strategies with different computational demands," and he doesn't believe that animals "are locked into one strategy or another." About the Speaker(s): Paul E.M. Phillips graduated in Physiology from the University of Liverpool in 1993. He then joined the Neurotransmission Research Group in the Academic Department of Anaesthesia and Intensive Care at St Bartholomew's and the Royal London School of Medicine and Dentistry (University of London) where he completed his Ph.D. in Neuroscience. In 1999 he moved to the University of North Carolina at Chapel Hill to take up a postdoctoral position in the Department of Chemistry. In 2003, he was appointed to Research Assistant Professor in that department. Phillips joined the faculty at the University of Washington in 2004. Host(s): School of Science, McGovern Institute for Brain Research at MIT
Imaging the Human Striatum and its Modulation by Dopamine
Imaging the Human Striatum and its Modulation by Dopamine Mon, 19 Dec 2011 13:27:45 -0500 05/07/2009 2:15 PM 46"3002Roshan Cools, Donders Institute for Brain, Cognition and Behavior Description: Researchers have known for some time that the neurotransmitter dopamine is centrally involved in learning and working memory, Roshan Cools tells us, and that dopamine"responsive circuits connect these parts of the human brain to other structures like the striatum, which also helps orchestrate motor control. Cools has been investigating in detail how dopamine acts within these cortico"striatal circuits to influence different types of cognitive processing. Specifically, Cools examined the effects of dopaminergic drugs (compounds that modulate the quantity of dopamine available to neurons, or the neurons' responsiveness to dopamine) on human subjects as they performed a variety of performance tasks. She notes that there's a "huge variability within and across individuals" to such drugs. The same chemical within the same subject may improve performance in one task, and impair it in another. The drug effect depends on an individual's baseline levels of dopamine: If someone starts with suboptimal levels, a dopamine"enhancing drug can restore someone to baseline, whereas someone starting with optimal levels of dopamine might be overdosed by the same drug. One of Cools' studies looked at the impact of dopaminergic drugs in Parkinson's disease (PD) patients, where "the primary pathology is dopamine depletion in the striatum." This depletion is not uniform, though, in the early and late stages of the disease, and impacts different sites in the striatum. Early stage PD patients suffer more from motor deficiencies than from higher level cortical deficiencies. Through performance tests and fMRI scans,Cools confirmed her hypothesis that in mild PD, dopamine"enhancing medication impaired performance on probabilistic reversal learning (a higher level cognitive task), "presumably by overdosing relatively intact levels of dopamine" in one part of the striatum. Yet these same drugs improved performance on other tasks associated with a part of the striatum concerned with motor systems. Cools has recently been testing healthy U.C. Berkeley undergrads with dopaminergic drugs, fMRI and PET scans, to see how levels of dopamine impact their performance on different learning tasks. Says Cools, "Dopaminergic medication improves reward" but impairs punishment"based learning in low"dopamine subjects and PD patients. Conversely, it improves punishment" but impairs reward"based reversal learning in high"dopamine subjects. This shift in the balance between reward" and punishment"based reversal likely reflects modulation by dopamine of striatal processing." About the Speaker(s): Roshan Cools completed her undergraduate degree in Experimental Psychology at the University of Groningen, The Netherlands, in 1998. She then moved to the University of Cambridge, where she earned an M. Phil. (1999), a Ph.D. (2002), a St John's College Junior Research Fellowship (2002"2006) and a Royal Society Dorothy Hodgkin Research Fellowship (2002 _ 2006). In 2003, Cools spent two post"doc years at U.C. Berkeley before moving back to Cambridge, where she obtained a Royal Society University Research Fellowship (2006 "2007). In November 2007 she returned to The Netherlands, where she studies the attentional and motivational control of decision"making and its modulation by dopamine and serotonin. Host(s): School of Science, McGovern Institute for Brain Research at MIT
The Power of Basic Science Applied to Medical Progress: Past Examples and Hope for Schizophrenia and Bipolar Illness
The Power of Basic Science Applied to Medical Progress: Past Examples and Hope for Schizophrenia and Bipolar Illness Fri, 16 Dec 2011 14:09:21 -0500 10/22/2009 4:00 PM 26"100Ed Scolnick, Director, Psychiatric Disease Program and the Stanley Center for Psychiatric Research, Broad InstituteDescription: An exemplar of the purpose"driven life in medical science, Ed Scolnick details research milestones from a remarkably varied career, revealing how scientific insight and collaborative effort translate into life"saving solutions for millions. This physician turned biochemist has held distinguished positions at the National Institutes of Health, Merck, and now at MIT, but common themes unite his pursuits: "I'm always excited by the inherent beauty of molecular and biochemical insights into how biology works. Making scientific discoveries for me is tremendously emotionally satisfying and in fact addicting." In his talk, Scolnick touches on such research breakthroughs as identifying virus oncogenes, and developing treatments for cardiovascular disease, Hepatitis B, and osteoporosis, among others. He emphasizes that teasing out the biochemistry of diseases is "the key to success in drug discovery." In Marfan syndrome, for example, investigators learned that a mutant gene leads to a malfunctioning aorta. Finding a cure flowed from understanding the underlying pathological processes. Scolnick proudly describes research on a gene involved with cholesterol buildup and an elevated risk for cardiovascular disease. This led to the development of statins, which has helped dramatically reduce the death rate in people with heart disease. Scolnick offers a dramatic chronology of his pioneering work at Merck starting in 1981 to find an effective AIDS treatment, an effort leading to the protease inhibitor Crixivan. His timeline covers more than a decade of scientific collaboration to block the mechanism of HIV, and involves false starts, the death of a key scientist in the Lockerbie bombing, pressure from AIDS activists and corporate overseers, a "miracle" AIDS patient, breakthroughs in measuring viral protein, and more than one "twist of fate." In 2004, Scolnick turned in a new direction: toward mental illness, a field stalled for decades due to ignorance "about the underlying biochemistry and physiology of the disease." Today, with the help of genomics and computative technologies, researchers are beginning to reveal the basic genetic architecture of schizophrenia and bipolar illness, says Scolnick. The "outline of their biochemistry" is starting to come clear for the first time, leading to the real possibility of novel therapeutics. While the challenges are formidable, he believes, consolidating MIT's "first rate neuroscience, human genetics, chemistry (creates) a unique opportunity to do something in a field that desperately needs the kind of approach and change we were able to bring to the AIDS field." NOTE: Audio levels for Kastner and Horvitz are very low, but improve when Scolnick begins his talk. We apologize for the inferior audio. About the Speaker(s): At the Broad Institute, Edward Scolnick works to identify risk genes for bipolar disorder and schizophrenia. From 1982"2003, Scolnick served as president of Merck Research Laboratories; executive vice president for science and technology at Merck & Company, Inc; executive director and vice president in the department of virus and cell biology and senior vice president for basic research at Merck Research Laboratories. Prior to joining Merck, he worked at the National Cancer Institute where he demonstrated the cellular origin of sarcoma virus oncogenes in mammals and defined specific genes that cause human cancer. He also worked at the National Heart Institute. Scolnick was elected to the National Academy of Sciences in 1984 and to the American Academy of Arts and Sciences in 1993. He became a member of the Institute of Medicine in 1996 and served on the Board of Directors of Merck & Co., Inc. from 1997 to 2002. He recently was selected as Regents' Lecturer, University of California at Berkeley, Frank H.T. Rhodes Class of '56 University Professor at Co[...]
Neural Basis of Drug Addiction
Neural Basis of Drug Addiction Fri, 16 Dec 2011 13:22:57 -0500 05/07/2009 4:15 PM 46"3002Barry Everitt, University of CambridgeDescription: How does someone move from recreational drug use to addiction? Barry Everitt's group at the University of Cambridge has been trying to break down the stages and neural circuitry of addiction with great precision. Everitt's research attempts to operationalize a progression in animals from the voluntary taking of drugs, to the acquired habit of drug"taking, to the stage of compulsive drug"seeking and consumption, "where individuals have really lost control." This progression seems rooted in the sequential activation of different learning systems in the brain, which are particularly sensitive to the neurotransmitter dopamine. Research suggests that drug"taking is initially dependent on the nucleus accumbens (part of the ventral striatum), but its establishment involves the dorsal striatum. Studies show that dopamine in the dorsal striatum is causally involved in establishing drug"seeking behavior in rats. As the animal gets accustomed to taking the cocaine, there's a "shift in the balance of associative encoding from ventral to dorsal striatum." Cocaine craving and self"administration seem to change the functioning of the dorsal striatum in monkeys and humans as well. While this shift from ventral to dorsal striatum depends to some degree on "pharmacology" (cocaine's impact on dopaminergic systems), Everitt has hypothesized that it may also involve "spiraling circuitry" connecting the ventral striatum, the midbrain -- the brain's motivational and motor mechanisms -- and the dorsal striatum. Everitt speculates that the compulsive nature of drug seeking may be rooted in part in the prefrontal cortex, home to "top"down executive control mechanisms." He describes research that attempted to model this type of compulsion. Animals with short"term access to cocaine and most animals with long"term access to cocaine suppressed their drug"seeking responses when punished. But a subgroup of 20% "persisted in seeking cocaine in the face of punishment." This result has been replicated many times now, and turns out to have a parallel among humans. This, says Everitt, "brings up the issue of vulnerability to drug addiction." Additional research suggests that impulsivity is a "behavioral characteristic that predicts the transition from initial drug intake to loss of control to compulsive seeking and taking" of drugs. Highly impulsive animals denied cocaine become more impulsive and drug seeking over time, leading to relapses. Everitt and others are tracing the neural basis of compulsivity to impairment in the prefrontal cortex, which involves "a loss of control over maladaptive habits" established after long"term drug taking. About the Speaker(s): Barry Everitt graduated in Zoology and Psychology at Hull University, received a Ph.D. from the University of Birmingham, and undertook post"doctoral research at Birmingham and at the Karolinska Institute in Stockholm. He was appointed to the Department of Anatomy at the University of Cambridge in 1974, became a Fellow of Downing College in 1976, a tenured University Lecturer and a Director of Studies in medicine at Downing in 1979. He has served on several national and international advisory committees and has been President of the British Association for Psychopharmacology, the European Brain and Behaviour Society and the European Behavioural Pharmacology Society. He is a Fellow of the Royal Society, a Fellow of the Academy of Medical Sciences, and has been awarded an Honorary D.Sc. by Hull University. Everitt's research concerns the neural and psychological mechanisms underlying learning, memory motivation and reward. Much of his current research involves the neuropsychology of drug addiction, especially drugs such as cocaine and heroin. A major research theme is the impact of learning on drug addiction " both its development and its persistence.Host(s): School of Science, McGovern Institute for Brain Rese[...]
Computational Models of Basal Ganglia Function
Computational Models of Basal Ganglia Function Fri, 16 Dec 2011 13:22:08 -0500 05/07/2009 1:30 PM 46"3002Kenji Doya, Okinawa Institute of Science and TechnologyDescription: As a mathematical engineer, Kenji Doya approaches the goal of describing the most intricate brain mechanisms from a computational perspective. He constructs models of reinforcement learning involving the networked structures of the basal ganglia. His efforts are captured and expressed quantitatively as probabilities, regressions, and algorithms. In this presentation, Doya covers basic concepts of reinforcement learning, then surveys the last decade of inquiry into the components of the basal ganglia circuit governing voluntary motion. Among the topics: action values, action candidates, and reward prediction involving the neurotransmitter dopamine; model"free versus model"based learning strategies; and the essential role of serotonin as modulator in the complex information loop. Doya's recent research is carried out via robots he calls "cyber rodents." His dream as an undergraduate was to "build a robot that learns the variety of behaviors on its own." That is, the computer, not the human engineer, teaches the robot to move. He accomplished this in designing a machine"creature exhibiting emotion"like attributes characterized as "depression," "impulsivity," "greed," and "patience." Doya believes the "metaparameters" of reinforcement learning must be "tuned appropriatelyOtherwise the performance of your learning is very, very poor." The iterative process involves three terms -- the reward itself, the expected reward for a new state based on choice of action, and memory of the reward gained in the previous state. In the comparison, any differential greater than zero can be exploited for learning. The tradeoff: "No pain, no gain." As research advanced to increasing levels of structural specificity, Doya posited that "there seems to be spatial segregation in the function" of basal ganglia components. Specialization in aspects of reinforcement learning is now seen, for instance, in ventral versus dorsal areas of the striatum. Differentiation is also found in the cortico"basal ganglia information network: not a simple closed loop, but parallel electrical pathways conducting distinct neural operations. Further, the neuromodulators each have their respective missions. Dopamine encodes the temporal difference error -- the reward learning signal. Acetylcholine affects learning rate through memory updates of actions and rewards. Noradrenaline controls width or randomness of exploration. Serotonin is implicated in "temporal discounting," evaluating if a given action is worth the expected reward. Doya reminds us that clinically "it is well known that the serotonin function is impaired in the depression patient." The system of basal ganglia components and neuromodulators requires dynamic balancing. A delicate interplay determines outcomes for learning, actions, and affective states. Doya's synthetic models are proxies for human behavior, and his computational framework describing the moving parts ultimately has therapeutic implications for psychiatric and neurological disorders. About the Speaker(s): Kenji Doya received B.S. and M.S. degrees from the University of Tokyo. His studies there culminated in a Ph.D. in Mathematical Engineering in 1991. He is Principal Investigator at the Okinawa Institute of Science and Technology in Japan, and is affiliated with the Advanced Telecommunications Research Institute International, heading the Computational Neuroscience Labs. Doya has concentrated on computational neurobiology to discover and describe through algorithms the molecular mechanisms of the mind. His research examines reinforcement learning, metalearning, sequence learning, neuromodulators, and specialization and integration of brain structures. His laboratory subjects have been birds, monkeys, rats, and robots he calls "cyber rodents." The past twenty years of Doya's research activities are documented in m[...]
What Harm Does Pathological Synchronization in Parkinson's Disease Do?
What Harm Does Pathological Synchronization in Parkinson's Disease Do? Fri, 16 Dec 2011 13:21:06 -0500 05/07/2009 11:15 AM 46"3002Peter Brown, Institute of Neurology, London Description: Like tuning in a station on the FM band of a radio, neuroscientists can detect the particular frequencies of our brains in action. And just as on the radio, a little noise and static is to be expected. In Parkinson's Disease (PD), as Peter Brown and colleagues are finding, too much of a certain type of frequency is a bad thing. Neurons in the basal ganglia produce a kind of overly synchronized beta frequency (in the 20 Hz range) that seems deeply implicated in some of the telltale symptoms of Parkinson's. Brown's talk outlines efforts to record this "oscillatory synchrony" in PD, to figure out the physiological mechanisms behind it, and to connect beta synchrony directly to such key symptoms in PD patients as rigidity and bradykinesia (slowness in executing movements). Scientists can detect clusters of neurons in the subthalamic nucleus (a key component of the basal ganglia) "beating" at 20 Hz. Brown says the "exaggerated synchrony" of these neurons seems to have something to do with a chronic loss of the neurotransmitter dopamine. Ordinary subjects have a "fair amount of healthy beta activity," notes Brown, and when these subjects engage in voluntary movements, such as extending a forefinger, the beta activity is suppressed. But in PD patients, says Brown, uncontrolled beta activity seems to promote postural contraction "at the expense of voluntary movement." Brown and others have recorded activity in the brains of PD patients undergoing two key treatments, Deep Brain Stimulation (where electrodes implanted in the brain try to break the pattern of normal neuronal firing) , and dopaminergic therapy. Both methods relieve the symptoms of slow movement and rigidity. Excessive beta oscillations are suppressed during these two treatments. This is "correlative evidence," says Brown, that beta activity is behind the symptoms. Scientists are trying to connect the dots, and find a causal link: After stimulating the neurons of the subthalamic nucleus to beat at 20 Hz, they observe a 20% slowing of movement. Brown is conducting additional studies that provide evidence in PD of a looping brain pathway involving not just the basal ganglia, but parts of the cortex, which has an "innate tendency for activity at 20 Hz," causing bradykinesia and rigidity, and which can be damped by the input of dopamine. In closing, Brown acknowledges he must bring "the beta story down to reality," since it doesn't seem to connect to other PD symptoms such as tremor, and "I've been a beta chauvinist here, and ignored other frequencies." About the Speaker(s): Peter Brown obtained his medical degree from Cambridge University in 1984 and then joined the Medical Research Council Human Movement and Balance Unit before moving to the Institute of Neurology, London. He works as a neurologist at the affiliated National Hospital for Neurology and Neurosurgery, and within the Sobell Department of Movement Disorders and Motor Neurophysiology at the Institute of Neurology, where he leads the Clinical Motor Neurophysiology Group. The principal objective of this group's research program is to define how activity in large populations of neurons is coordinated in healthy movement and how such coordination may go awry in diseases, particularly those of the basal ganglia such as Parkinson's disease. Host(s): School of Science, McGovern Institute for Brain Research at MIT
Deep Brain Stimulation Therapy for Movement Disorders
Deep Brain Stimulation Therapy for Movement Disorders Fri, 16 Dec 2011 13:19:36 -0500 05/07/2009 10:30 AM 46"3002Andres Lozano, University of Toronto Description: New tools are enabling neuroscientists to break therapeutic ground against daunting disorders like Parkinson's Disease (PD). Andres Lozano is one "of a small group of heroes," in Ann Graybiel's estimate, whose work is yielding astonishing advances on a variety of fronts. Treatments for PD, a progressive, degenerative brain disorder, have until recently dealt primarily with the loss of dopamine"releasing neurons, leading to the classic movement disorders associated with PD: tremor, rigidity, akinesia. But Lozano says that by the time these physical problems are diagnosed, "the reality is that the disease started 10"15 years earlier," and has involved other brain areas. Lozano determined to focus on three such non"motor symptoms of the disease -- gait and posture, depression (in PD and other patients), and cognitive disorders -- and if possible, "reach these circuits, intervene and help patients." PD patients have serious problems controlling balance and posture, and animal studies helped pinpoint an area in the brainstem responsible for these functions. Lozano got permission to plant electrodes in humans in this area, and mapped out the sensitivities of neurons to voluntary movements such as flexing an ankle or walking. In six PD patients, Lozano sent a mild electric current into these neurons. He shows videos demonstrating the remarkable improvement in control (a patient pushed no longer falls) with deep brain stimulation (DBS). A serendipitous offshoot of this therapy is that it improves REM sleep, in which PD patients are deficient. Lozano has been working as well on mapping and targeting areas of the brain involved in depression, which he has found to be hyperactive. He labeled neurons that responded exclusively to sad and disturbing images, and using DBS, he was able to "turn down the hyperactivity," successfully reversing severe depression in 60% of his 36 subjects. His final accomplishment emerged by accident: While attempting to treat a patient's morbid obesity through DBS, Lozano was startled to find when stimulating the man's thalamus the patient experienced a vivid sense of d_j_ vu. (He recalled being in a field 30 years earlier with a girlfriend.) The stronger the current, the more details emerged. When the stimulus ended, the memory ceased. Lozano hopes, via DBS, to help patients with memory disorders. Another intriguing discovery: stimulation in the hippocampus, deeply involved in memory, seems to lead to a burst of new neuron development. These DBS studies suggest, says Lozano, that brain circuits for mood, motor control and cognition can be modulated, and we now "need to determine whether they are safe and beneficial to patients." About the Speaker(s): Andres Lozano works on novel surgical approaches to treat Parkinson's disease, depression and Alzheimer's disease. His labs use brain imaging, electrophysiology and surgical techniques. The work in humans is complemented by laboratory work involving cell death in Parkinson's disease, effects of stimulation on hippocampal neurogenesis and animal models of deep brain stimulation. A graduate of the University of Ottawa, Faculty of Medicine in 1983, Lozano underwent Neurosurgical Training at McGill University. He became a Fellow of the Royal College of Physicians and Surgeons of Canada in 1990. During his residency in Montreal, Lozano earned his Ph.D. in Experimental Medicine in 1989. He joined the Neurosurgical Staff at the Toronto Western Hospital in 1991. Host(s): School of Science, McGovern Institute for Brain Research at MIT
Representation of Value in the Primate Brain
Representation of Value in the Primate Brain Fri, 16 Dec 2011 13:18:11 -0500 05/07/2009 9:15 AM 46"3002Paul Glimcher, New York University Description: Pigeons really like millet seed, monkeys crave juice, and humans get a kick out of winning money. While all animals don't enjoy the same rewards, Paul Glimcher has discovered some common features in the way animal brains learn to recognize and pursue something of value. Glimcher is one of the founding fathers of the young field of neuroeconomics, in which economic theories help inform investigations of brain function. It's not surprising then, that his approaches include game theory as well as measuring the firing of single neurons. Glimcher's talk details his research from the past 15 years, what he describes as an attempt to "add something" to the classic studies on the basal ganglia circuit conducted by fellow symposium speaker Okihide Hikosaka. From Hikosaka's data and other research, Glimcher came to believe that neurons of the substantia nigra (part of the basal ganglia) were coding for something of worth to an animal, but that these neurons were "responding not to reward per se, but to deviations to expectation." For instance, if a pigeon expected a delivery of millet seed following a conditioned cue, no neurons fired, but if the reward was delayed, then suddenly delivered, the pigeon would find its initial prediction in error, and its neurons burst into action. Various models emerged to capture the ways in which these neurons, energized primarily by the neurotransmitter dopamine, enabled animals to adjust expectations about and predict rewards. But Glimcher found fault with others scientists' "conditional parameters." He says, "As an economist, this is frustrating." So he developed three mathematical axioms for testing the so"called Reward Prediction Error (RPE) models. His work "suggested a way of unifying the data," with the notion that the basal ganglia learns "the values of actions in a quantitative way from the dopamine neurons and the incoming stimulus." Glimcher hypothesized that dopamine neurons take the value of a reward just received, "and subtract it from a weighted exponential average of previous rewards, and if there's no mismatch, there should be no firing ofdopamine neurons." Human, monkey and pigeon studies -- based on gambling, juice, and seed rewards, respectively -- solidified his notion that dopamine neurons are part of an RPE encoding system where they convey the differences between rewards expected and rewards received. This has led Glimcher to believe that "one of the principle functions of the basal ganglia is to learn the values of our actions, represent them, and pump out the data to produce choice." About the Speaker(s): Paul Glimcher has focused for the past decade on identifying and characterizing the signals that intervene between the neural processes involved with sensory encoding, and the neural processes involved in generating movement -- the signals, he says, that in principle underlie decision"making. Glimcher came to New York University from the University of Pennsylvania, where he earned his Ph.D. in Neuroscience in 1989, and where he served as a postdoctoral research fellow. He graduated from Princeton University with an A.B. in Neuroscience in 1983. Glimcher is a member of the Society for Neuroscience, the American Economic Association, the Society for Neuroeconomics (of which he was founding president), and AAAS. He is the author of Neuroeconomics: Decision Making and the Brain(Elsevier, 2008), and Decisions, Uncertainty, and the Brain: The Science of Neuroeconomics (MIT Press, 2004), among other books and publications. Host(s): School of Science, McGovern Institute for Brain Research at MIT
How the Brain Encodes Reward
How the Brain Encodes Reward Fri, 16 Dec 2011 13:16:26 -0500 05/07/2009 8:30 AM 46"3002Okihide Hikosaka, National Eye Institute Description: As Ann Graybiel puts it, "basal ganglia were dark basement structures" until Okihide Hikosaka began his classic 1980s research demonstrating how these neuronal clusters influenced eye movements. Hikosaka has deepened and broadened his work in this once neglected area of the brain, and brings a McGovern audience up to date on his latest discoveries. Hikosaka briefly sketches what is known about the basic pathways leading in, around and out of the basal ganglia, circuits that have been associated with stress, pain, mood, memory and arousal. This specialized cluster of neurons seems especially attuned to the neurotransmitter dopamine, and Hikosaka has been investigating "a number of unsolved questions," including how dopamine neurons form circuits for movement control, whether such neurons encode "motivational values," and what other parts of the brain guide them. Hikosaka describes research demonstrating that certain dopamine neurons become excited if a visual cue indicates a future reward, and become inhibited with a visual cue indicating no reward. Dopamine also increases after an action delivers a reward and decreases when an action produces no reward. Research began to explore whether dopamine neurons "encode motivational values, including reward and punishment." After others' studies yielded contradictory or uncertain conclusions, Hikosaka designed a set of studies on monkeys involving classical Pavlovian conditioning, with juice rewards and air puffs as aversive stimuli. Among Hikosaka's findings: some dopamine neurons were excited primarily by positive, reward"predicting stimuli, others inhibited by air puff"predicting stimuli. But he also found another group of dopamine neurons excited both by positive and negative reward"predicting stimuli (as well as the stimuli themselves). Hikosaka posited two types of neurons that react in very different ways to motivational signals, which he described as value"coding and salience"coding. He also determined that the lateral habenula, a part of the brain sitting at one end of the thalamus, seems to regulate dopamine pathways involved in some motivational responses. By sending a weak electric pulse through the lateral habenula, Hikosaka saw a very strong inhibition of the dopamine neurons that "encode mostly motivational values." About the Speaker(s): Okihide Hikosaka researches the control of eye movements, functions of the basal ganglia, neural mechanisms of motivation, neural mechanisms of procedural learning, and mechanisms of spatial attention. Hikosaka earned a graduate degree at the University of Tokyo in 1978, and became a Lecturer at Toho University School of Medicine. From 1979"1982, he was a visiting scientist at the National Eye Institute. In 1983, he was named Associate Professor at Toho University School of Medicine. In 1988, he became a Professor at the National Institute of Physiological Sciences in Okazaki, and from 1993"2002, he was a Professor at Juntendo University School of Medicine. He joined the Laboratory of Sensorimotor Research, National Eye Institute at NIH in 2002. Host(s): School of Science, McGovern Institute for Brain Research at MIT
Parkinson's Disease: Hope Through Research
Parkinson's Disease: Hope Through Research Fri, 21 Oct 2011 16:32:39 -0400 (01:21:48) On Thursday, October 20th, leading experts from the McGovern Institute for Brain Research at MIT and the American Parkinson Disease Association discussed cutting edge advances in Parkinson's disease research and provided perspective on what the future holds for Parkinson's patients and their families.Speakers: Roberta Sydney SM '88: Chair, Friends of the McGovern Institute Ann Graybiel, PhD: Investigator, McGovern Institute Marie Saint-Hilaire, MD, FRCPC: Director, Parkinson’s Disease and Movement Disorders Center and the APDA Center for Advanced Research at Boston University Medical Center Following the formal presentations, guests participated in an open floor discussion with the speakers.
Alan Jasanoff: Novel MRI sensor provides molecular view of brain
Alan Jasanoff: Novel MRI sensor provides molecular view of brain Fri, 19 Feb 2010 15:24:01 -0500 Alan Jasanoff is developing a new generation of brain imaging technologies to study the neural mechanisms of behavior. In this video press release, Jasanoff discusses his latest findings published in Nature Biotechnology on February 28, 2010. In this study, Jasanoff's team designed a new MRI sensor that responds to the neurotransmitter dopamine, an achievement that may significantly improve the specificity and resolution of future brain imaging procedures.For more information about the McGovern Institute, please visit our website: http://mcgovern.mit.edu
Meet Alan Jasanoff
Meet Alan Jasanoff Tue, 09 Feb 2010 16:38:23 -0500 (5:06) Functional magnetic resonance imaging (fMRI) has revolutionized our understanding of the human brain, but the method is now approaching the limit of its capabilities. Alan Jasanoff hopes to break through this limit and to develop new technologies for imaging the molecular and cellular phenomena that underlie brain function.Learn more about Alan Jasanoff>> [Stock footage courtesy pond5]
Class 14 | Introduction to Cognitive Neuroscience - Summer 2008
Class 14 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 23 Jul 2009 13:59:28 -0400 In this session: Learning and long term potentiationThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 19 | Introduction to Cognitive Neuroscience - Summer 2008
Class 19 | Introduction to Cognitive Neuroscience - Summer 2008 Wed, 10 Jun 2009 13:29:09 -0400 Language and the brain
Class 16 | Introduction to Cognitive Neuroscience - Summer 2008
Class 16 | Introduction to Cognitive Neuroscience - Summer 2008 Wed, 10 Jun 2009 13:26:20 -0400 In this session: Numbers and mathThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 22 | Introduction to Cognitive Neuroscience - Summer 2008
Class 22 | Introduction to Cognitive Neuroscience - Summer 2008 Tue, 26 May 2009 10:46:40 -0400 In this session: Alzheimer's diseaseThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 21 | Introduction to Cognitive Neuroscience - Summer 2008
Class 21 | Introduction to Cognitive Neuroscience - Summer 2008 Tue, 26 May 2009 10:34:47 -0400 In this session: Some thoughts about musicThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 20 | Introduction to Cognitive Neuroscience - Summer 2008
Class 20 | Introduction to Cognitive Neuroscience - Summer 2008 Tue, 26 May 2009 10:21:18 -0400 In this session: Language productionThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 18 | Introduction to Cognitive Neuroscience - Summer 2008
Class 18 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 16:03:38 -0400 In this session: Language processingThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 17 | Introduction to Cognitive Neuroscience - Summer 2008
Class 17 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 15:56:29 -0400 In this session: Auditory perceptionThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 15 | Introduction to Cognitive Neuroscience - Summer 2008
Class 15 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 15:20:25 -0400 In this session: Number processingThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 12 | Introduction to Cognitive Neuroscience - Summer 2008
Class 12 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 13:54:08 -0400 In this session: Working memory IIThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 11 | Introduction to Cognitive Neuroscience - Summer 2008
Class 11 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 13:38:28 -0400 In this session: Working memory IThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 10 | Introduction to Cognitive Neuroscience - Summer 2008
Class 10 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 12:29:06 -0400 In this session: Attention IIThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 9 | Introduction to Cognitive Neuroscience - Summer 2008
Class 9 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 12:08:50 -0400 In this session: Attention IThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 7 | Introduction to Cognitive Neuroscience - Summer 2008
Class 7 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 12:02:55 -0400 In this session: Visual processingThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 2 | Introduction to Cognitive Neuroscience - Summer 2008
Class 2 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 11:57:59 -0400 In this session: Nervous systemThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
Class 1 | Introduction to Cognitive Neuroscience - Summer 2008
Class 1 | Introduction to Cognitive Neuroscience - Summer 2008 Thu, 21 May 2009 11:51:27 -0400 In this session: Overview of cognitionThought, learning, perception, reasoning, and language are all cognitive abilities powered by the soft squishy gray stuff inside our skulls. After a quick-and-dirty introduction to neurons and the brain, we'll examine several aspects of human cognition and look at the neurophysiology that underlies them. We'll also discuss methods used to study these areas, read some current research, and navigate the wilds of the science library.
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