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  • the amygdala that assign emotions to experience How the brain tells good from bad Eating a slice of chocolate cake or spending time with a friend usually stimulates positive feelings while getting in a car accident or anticipating a difficult exam is more likely to generate a Read More 0 By Joshua Sarinana In Publications Sur Lab Publications Posted April 27 2015 An acetylcholine activated microcircuit drives temporal dynamics of cortical activity Chen N Sugihara H Sur M 2015 Nat Neurosci 18 6 892 902 Read More 0 By Joshua Sarinana In News Press Releases Sur Lab News Posted April 27 2015 Picower researchers ID brain mechanisms underlying alertness and attentiveness CAMBRIDGE Mass Researchers at MIT s Picower Institute for Learning and Memory show for the first time that a common neurotransmitter acts via a single type of neuron to enable the Read More 0 By Joshua Sarinana In Featured News News Press Releases Tsai Lab News Posted April 22 2015 Alana Foundation gift to support study of Down syndrome MIT and Case Western Reserve University have each received 1 7 million from Brazil s Alana Foundation to develop a collaboration that will help advance our understanding of Down syndrome The Read More 0 By Joshua Sarinana In Miller Lab Publications Publications Posted April 18 2015 Frequency specific hippocampal prefrontal interactions during associative learning Brincat SL Littleton EK Nat Neurosci 2015 Apr 18 4 576 81 doi 10 1038 nn 3954 Epub 2015 Feb 23 Read More 0 By Joshua Sarinana In Featured News Heiman Lab News Lab News News Posted April 6 2015 Novel research technique suggests an antioxidant gene protects vulnerable neurons Researchers have developed a new technique that allows them to screen for genes that could contribute to the progression of Huntington s disease and other neurodegenerativedisorders

    Original URL path: https://picower.mit.edu/cms/2015/04/ (2016-04-25)
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  • being in sync is a good thing The attentive brain surprisingly is not one of them Decorrelation neurons firing in an unsynchronized manner can enhance and even optimize information processing In fact conditions such as Parkinson s disease and epilepsy are characterized by pathologically synchronized neurons The Picower study pinpoints for the first time a specific subtype of inhibitory neuron that contributes to decorrelation in a major brain circuit tied to attention and arousal The mechanisms underlying ACh modulated brain functions are complex due to the sheer number of types of brain cells that ACh modulates said former graduate student Naiyan Chen co author of the paper Surprisingly we found a single cell type is responsible for ACh based information representation in the brain This study intended to shed light on brain function at the circuit level is the first to demonstrate a crucial emerging principle of cortical circuits that the diffuse release of ACh within the cortex previously thought to contribute to nonspecific actions actually leads to highly specific functions Sur said Certain cells have receptors that are finely tuned to such transmitters and these cells are in turn part of specific circuits This enables neurotransmitter systems and cortical circuits to create very specific response transformations that underlie cognitive functions such as attention and brain states that accompany alertness and arousal he said Naiyan and research scientist Hiroki Sugihara demonstrated these circuits and their function in genetically modified mice by recording the actions of specific neurons and activating and inactivating different neuron classes to deconstruct their roles Chen anticipates that these findings will motivate future research in other brain functions such as learning and plasticity modulated by the neurotransmitter acetylcholine An interesting next question is Do different acetylcholine modulated cell types mediate different brain functions she said This work

    Original URL path: https://picower.mit.edu/cms/20150427/picower-researchers-id-brain-mechanisms-underlying-alertness-and-attentiveness/ (2016-04-25)
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  • nearly two decades investigating the biological underpinnings of Down syndrome and searching for potential drug therapies to enhance cognition and prevent the development of Alzheimer s related dementia in persons with this condition He is also working to bring this research into the clinical arena There is tremendous opportunity to benefit from our combined strengths MIT s ongoing research to understand the aging brain and Case Western Reserve s expertise in Down syndrome says Tsai who is also the Picower Professor of Neuroscience in MIT s Department of Brain and Cognitive Sciences The Alana Foundation s support will allow us to work together to accelerate research projects with the potential to develop treatments that will improve the quality of life for individuals with Down syndrome As they age individuals with Down syndrome have a greatly increased risk of developing a type of dementia that is very similar to that seen in Alzheimer s disease One of the many questions that Tsai and Costa hope to answer about Down syndrome is whether insights gained from work on Alzheimer s disease can help shed light on Down syndrome The rationale is that therapeutic strategies that Tsai has discovered for Alzheimer s disease may be beneficial for Down syndrome and vice versa This is a unique collaborative effort that makes the best possible use of the complementary expertise of our research teams Professor Tsai and I feel privileged to be the recipients of this generous gift from the Alana Foundation says Costa a professor of pediatrics at Case Western Reserve The collaboration will focus initially on four project areas First Tsai and Costa will develop personalized human stem cell models of Down syndrome called iPSCs induced pluripotent stem cells iPSCs are nonspecialized cells that can be induced to develop into many different types of mature cells such as neurons Researchers can then study these induced human neuronal models of Down syndrome to better understand the biology of the condition Second the team will use this human neuronal model of Down syndrome to test the benefits of potential new therapeutic treatments This could provide a preclinical drug screening approach that is personalized to individual conditions In another project Tsai and Costa will breed mice that are genetically protected from Alzheimer s disease with mice that mimic Down syndrome to determine if the same pathological processes that are at work in Alzheimer s disease occur in Down syndrome Tsai has recently shown that limiting the expression of the protein p25 in mouse models of Alzheimer s disease can slow the progression of many hallmark symptoms and cognitive impairments of the condition Therefore the teams will explore whether the mice that mimic Down syndrome could benefit from the same protein regulation The model will also be used to test the effectiveness of Tsai s newly discovered class of cognitive enhancers called HDAC inhibitors which can benefit the cognitive function of mouse models of Alzheimer s disease In a fourth project the teams will use a new

    Original URL path: https://picower.mit.edu/cms/20150422/alana-foundation-gift-to-support-study-of-down-syndrome/ (2016-04-25)
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  • Institute for Learning and Memory and senior author of a paper describing the findings in the Feb 23 online edition of Nature Neuroscience Furthermore these oscillations may reinforce the correct guesses while repressing the incorrect guesses helping the brain learn new information the researchers say Signaling right and wrong Miller and lead author Scott Brincat a research scientist at the Picower Institute examined activity in the brain as it forms a type of memory called explicit memory memory for facts and events This includes linkages between items such as names and faces or between a location and an event that took place there During the learning task animals were shown pairs of images and gradually learned through trial and error which pairs went together Each correct response was signaled with a reward As the researchers recorded brain waves in the hippocampus and the prefrontal cortex during this task they noticed that the waves occurred at different frequencies depending on whether the correct or incorrect response was given When the guess was correct the waves occurred in the beta frequency about 9 to 16 hertz cycles per second When incorrect the waves oscillated in the theta frequency about 2 to 6 hertz Previous studies by MIT s Mark Bear also a member of the Picower Institute have found that stimulating neurons in brain slices at beta frequencies strengthens the connections between the neurons while stimulating the neurons at theta frequencies weakens the connections Miller believes the same thing is happening during this learning task When the animal guesses correctly the brain hums at the correct answer note and that frequency reinforces the strengthening of connections he says When the animal guesses incorrectly the wrong buzzer buzzes and that frequency is what weakens connections so it s basically telling the brain to forget about what it just did The findings represent a major step in revealing how memories are formed says Howard Eichenbaum director of the Center for Memory and Brain at Boston University This study offers a very specific detailed story about the role of different directions of flow who s sending information to whom at what frequencies and how that feedback contributes to memory formation says Eichenbaum who was not part of the research team The study also highlights the significance of brain waves in cognitive function which has only recently been discovered by Miller and others Brain waves had been ignored for decades in neuroscience It s been thought of as the humming of a car engine Miller says What we re discovering through this experiment and others is that these brain waves may be the infrastructure that supports neural communication Enhancing memory The researchers are now investigating whether they can speed up learning by delivering noninvasive electrical stimulation that oscillates at beta frequencies when the correct answer is given and at theta frequencies when the incorrect answer is given The idea is that you make the correct guesses feel more correct to the brain and the incorrect guesses

    Original URL path: https://picower.mit.edu/cms/20150223/how-brain-waves-guide-memory-formation/ (2016-04-25)
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  • epigenomic signals in mice and humans reveal immune basis of Alzheimer s disease Gjoneska E Pfenning A R Mathys H Quon G Kundaje A Tsai L H Kellis M 2015 Nature 518 7539 365 9 Read More 1 By Joshua Sarinana In News Posted February 19 2015 Xu Liu in Memoriam Extending our condolences to family friends and colleagues the MIT community and the Picower Institute for Learning and Memory are deeply saddened by this week s sudden passing of Xu Liu Xu Read More 0 By Joshua Sarinana In Press Releases Tsai Lab News Posted February 16 2015 Epigenomics of Alzheimer s Disease Progression Study of epigenomic modifications reveals immune basis of Alzheimer s disease Our susceptibility to disease depends both on the genes that we inherit from our parents and on our lifetime Read More 0 By Joshua Sarinana In Bear Lab Publications Publications Posted February 15 2015 Microchip amplifier for in vitro in vivo and automated whole cell patch clamp recording Harrison R R Kolb I Kodandaramaiah S B Chubykin A A Yang A Bear M F Boyden E S Forest C R 2015 J Neurophysiol 113 4 1275 82 Read More 0 By Joshua Sarinana In Featured News Lab News Media Mentions News Tsai Lab News Posted February 15 2015 Catalog of DNA modifications produces surprises A series of fine tuned maps of DNA packaging in human cells reveal dynamic new views of how the genome s instructions are carried out to build a person The maps also offer surprising insights Read More 0 By Joshua Sarinana In Publications Wilson Lab Publications Posted February 11 2015 Phase organization of network computations Wilson M A Varela C Remondes M 2015 Curr Opin Neurobiol 31 250 3 Read More 0 By Joshua Sarinana In Publications Tsai Lab Publications

    Original URL path: https://picower.mit.edu/cms/2015/02/ (2016-04-25)
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  • known as microglia which are responsible for clearing away infected or damaged cells They also secrete chemicals that produce inflammation Our data suggest that microglia are heavily activated during Alzheimer s disease progression although it is unknown exactly how they contribute to the disease Tsai says These cells are important for normal brain function and share their key cell surface markers CD14 with macrophages that infiltrate the brain from elsewhere in the body during disease progression Conserved epigenomic signatures The researchers then compared the results in mice with what is known about Alzheimer s disease in humans They found that differences in gene levels in the Alzheimer s like mouse brain matched differences previously seen in the brains of Alzheimer s patients which prompted them to ask if the epigenetic signatures might also be conserved The researchers found that this was the case specifically the same regulatory regions that were active or repressed in mice showed the same patterns in humans They also found that the regions with increased activity in the mouse model of Alzheimer s disease had immune functions in humans and the regions that showed decreased activity had neural functions in humans Our results show that functional conservation between human and mouse is not restricted to protein coding genes says Andreas Pfenning joint first author of the study and a postdoc at MIT This opens up the use of epigenomics methods in model organisms to study an inaccessible organ like the brain and how it changes in response to activity or disease Genetic variants cluster in immune pathways Previous studies of the genomes of Alzheimer s patients had identified common genetic variants associated with the disease but scientists did not know how these DNA variants could contribute to the disease since the majority of them are found outside of protein coding regions Our conserved epigenomic maps allowed us to now place these noncoding genetic variants in the context of disease relevant regulatory regions and interpret their contribution to the disease predisposition Kellis says As inherited common genetic variants always precede disease onset they are always indicative of causal roles and thus can shed additional light on the epigenomic alterations The researchers found that genetic variants associated with Alzheimer s disease were only associated with immune processes and not with neural processes indicating that genetic predisposition to Alzheimer s disease primarily affects the circuitry of immune processes rather than neuronal processes Our results suggest that repression of neural pathways does not represent genetic predisposition even though it is a hallmark of Alzheimer s Tsai says Instead it may occur as a consequence of environmental factors and aging and result from interactions with the altered immune pathways The researchers identified a small number of master regulators that target many of the regulatory regions that overlap Alzheimer s associated genetic variants in humans Among these PU 1 targets a large number of altered regulatory regions and the genetic region encoding PU 1 is associated with Alzheimer s disease suggesting PU

    Original URL path: https://picower.mit.edu/cms/20150216/epigenomics-of-alzheimers-disease-progression/ (2016-04-25)
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  • is mediated by a different neural circuit than physiological healthy eating For the study Tye and her graduate student Edward Nieh focused on the connections between the VTA and the lateral hypothalamus LH which controls feeding But because the LH also controls diverse other behaviors and connects to multiple other brain regions no one had yet isolated a feeding and reward processing circuit Tye and Nieh first identified and characterized just the LH neurons that connect to the VTA and recorded their naturally occurring activities in brain slices with the help of Gillian Matthews before moving to animal experiments Electrodes recorded the activity of these identified neurons during animal behaviors Mice naturally love sucrose similar to humans loving sugar rich sodas so Nieh trained mice to seek out sucrose at a delivery port upon hearing and seeing a cue After the mice learned to predict a sucrose reward upon cue he randomly withheld the reward about half the time a bitter disappointment Other times the mice unexpectedly received a sucrose reward without any predictive cue a sweet surprise This difference between the expectation and the experience is called the reward prediction error The neural recordings showed that one type of LH neurons connecting to the VTA only became active after the animal had learned to seek a sucrose reward whether or not it actually received the reward Another set of LH neurons upon receiving feedback from the VTA encoded the response to the reward or to its omission Next Nieh worked with an MD PhD student in Tye s lab Stephen Allsop to modify mice so that the LH VTA neural projections carried light sensitive proteins that can activate or silence neurons with pulses of light a method called optogenetics Activating the projections led to compulsive sucrose eating and increased overeating in mice that were full Inactivating this pathway reduced the compulsive sucrose seeking that resembles addiction but did not prevent mice that were hungry from eating regular chow That was exciting because we have the recording data to show how this compulsive sugar seeking happens Nieh says and we can drive or suppress just the compulsive behavior by making very precise changes in the neural circuit Addiction researchers have hypothesized that the transition from actions to habits to compulsion is the path to addiction formation but exactly where and how this happens in the brain has been a mystery says Tye who is also the Whitehead Career Development Assistant Professor in MIT s Department of Brain and Cognitive Sciences Now we have evidence showing that this transition is represented in the LH VTA circuit Nieh working with Matthews a postdoc in the Tye lab also showed that the LH neurons send a mix of excitatory glutamate and inhibitory GABA signals to the VTA But contrary to expectation it was the inhibitory signals not the excitatory ones that triggered the feeding activity in the mice When GABA projections alone were activated the mice behaved bizarrely gnawing on the bottom of

    Original URL path: https://picower.mit.edu/cms/20150129/separate-neural-circuits-control-sugar-cravings-and-healthy-eating/ (2016-04-25)
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  • Lab News Media Mentions Miller Lab News News Posted January 21 2015 Multi tasking and technology Professor Earl Miller Getting back into work routines after a holiday break is something many of us will already have come to grips with in recent weeks And these routines seem to get busier all the time as modern Read More 0 By Joshua Sarinana In Bear Lab News Press Releases Posted January 20 2015 MIT Researchers Find where Visual Memories are Made Discovery could lead to new treatments for cognitive disorders including autism and schizophrenia In findings that may lead to new treatments for cognitive disorders researchers at MIT s Read More 0 By Joshua Sarinana In Bear Lab Publications Publications Posted January 19 2015 Visual recognition memory manifested as long term habituation requires synaptic plasticity in V1 Cooke S F Komorowski R W Kaplan E S Gavornik J P Bear M F 2015 Nat Neurosci 18 2 262 71 Epub 2015 Jan 19 Read More 0 By Joshua Sarinana In Bear Lab News Featured News Lab News Media Mentions News Posted January 19 2015 Drug abates symptoms in two genetic models of autism Drugs developed to treat fragile X syndrome may also work for autism because both disorders feature defects at neuronal junctions or synapses suggests a paper published 12 January in Nature Read More 0 By Joshua Sarinana In Publications Tye Lab Publications Posted January 15 2015 From circuits to behaviour in the amygdala Janak P H Tye K M 2015 Nature 517 7534 284 92 Read More 0 By Joshua Sarinana In Publications Tye Lab Publications Posted January 15 2015 In vivo optogenetic stimulation of the rodent central nervous system Sidor M M Davidson T J Tye K M Warden M R Diesseroth K McClung C A 2015 J Vis Exp 95 51483 in press Read More 0 By Joshua Sarinana In Publications Wilson Lab Publications Posted January 13 2015 Optogenetic activation of cholinergic neurons in the PPT or LDT induces REM sleep Van Dort C J Zachs D P Kenny J D Zheng S Goldblum R R Gelwan N A Ramos D M Nolan M A Wang K Weng F J Lin Y Wilson M A Brown E N 2015 Proc Natl Acad Sci USA Read More 0 By Joshua Sarinana In Bear Lab News Press Releases Posted January 12 2015 New Findings Reveal Genetic Brain Disorders Converge at the Synapse Picower Institute researchers show that different causes of autism and intellectual disability respond to the same treatment Several genetic disorders cause intellectual disability and autism Read More 0 By Joshua Sarinana In Bear Lab Publications Publications Posted January 12 2015 Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11 2 microdeletion Tian D Stoppel L J Heynen A J Lindemann L Jaeschke G Mills A A Bear M F 2015 Nat Neurosci 18 2 182 4 Read More 0 By Joshua Sarinana In Publications Tye Lab Publications Posted January 6 2015 Daytime spikes in

    Original URL path: https://picower.mit.edu/cms/2015/01/ (2016-04-25)
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