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  1. Article: Somatic cancer driver mutations are enriched and associated with inflammatory states in Alzheimer's disease microglia.

    Huang, August Yue / Zhou, Zinan / Talukdar, Maya / Miller, Michael B / Chhouk, Brian / Enyenihi, Liz / Rosen, Ila / Stronge, Edward / Zhao, Boxun / Kim, Dachan / Choi, Jaejoon / Khoshkhoo, Sattar / Kim, Junho / Ganz, Javier / Travaglini, Kyle / Gabitto, Mariano / Hodge, Rebecca / Kaplan, Eitan / Lein, Ed /
    De Jager, Philip L / Bennett, David A / Lee, Eunjung Alice / Walsh, Christopher A

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Alzheimer's disease (AD) is an age-associated neurodegenerative disorder characterized by progressive neuronal loss and pathological accumulation of the misfolded proteins amyloid-β and ... ...

    Abstract Alzheimer's disease (AD) is an age-associated neurodegenerative disorder characterized by progressive neuronal loss and pathological accumulation of the misfolded proteins amyloid-β and tau
    Language English
    Publishing date 2024-01-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.03.574078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity.

    Fong, Ming-Fai / Finnie, Peter Sb / Kim, Taekeun / Thomazeau, Aurore / Kaplan, Eitan S / Cooke, Samuel F / Bear, Mark F

    Cerebral cortex (New York, N.Y. : 1991)

    2020  Volume 30, Issue 4, Page(s) 2555–2572

    Abstract: Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification ... ...

    Abstract Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1. We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity. We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells. We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity.
    MeSH term(s) Animals ; Evoked Potentials, Visual/physiology ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Neuronal Plasticity/physiology ; Photic Stimulation/methods ; Receptors, N-Methyl-D-Aspartate/deficiency ; Receptors, N-Methyl-D-Aspartate/genetics ; Sensory Deprivation/physiology ; Visual Cortex/physiology
    Chemical Substances Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2020-07-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1077450-6
    ISSN 1460-2199 ; 1047-3211
    ISSN (online) 1460-2199
    ISSN 1047-3211
    DOI 10.1093/cercor/bhz260
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  3. Article ; Online: Visual recognition memory, manifested as long-term habituation, requires synaptic plasticity in V1.

    Cooke, Sam F / Komorowski, Robert W / Kaplan, Eitan S / Gavornik, Jeffrey P / Bear, Mark F

    Nature neuroscience

    2015  Volume 18, Issue 2, Page(s) 262–271

    Abstract: Familiarity with stimuli that bring neither reward nor punishment, manifested through behavioral habituation, enables organisms to detect novelty and devote cognition to important elements of the environment. Here we describe in mice a form of long-term ... ...

    Abstract Familiarity with stimuli that bring neither reward nor punishment, manifested through behavioral habituation, enables organisms to detect novelty and devote cognition to important elements of the environment. Here we describe in mice a form of long-term behavioral habituation to visual grating stimuli that is selective for stimulus orientation. Orientation-selective habituation (OSH) can be observed both in exploratory behavior in an open arena and in a stereotyped motor response to visual stimuli in head-restrained mice. We found that the latter behavioral response, termed a 'vidget', requires V1. Parallel electrophysiological recordings in V1 revealed that plasticity, in the form of stimulus-selective response potentiation (SRP), occurred in layer 4 of V1 as OSH developed. Local manipulations of V1 that prevented and reversed electrophysiological modifications likewise prevented and reversed memory demonstrated behaviorally. These findings suggest that a form of long-term visual recognition memory is stored via synaptic plasticity in primary sensory cortex.
    MeSH term(s) Animals ; Behavior, Animal/physiology ; Electrophysiological Phenomena/physiology ; Evoked Potentials, Visual/physiology ; Habituation, Psychophysiologic/physiology ; Male ; Memory, Long-Term/physiology ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity/physiology ; Pattern Recognition, Visual/physiology ; Somatosensory Cortex ; Visual Cortex/cytology ; Visual Cortex/physiology
    Language English
    Publishing date 2015-01-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.3920
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  4. Article ; Online: Erratum: Visual recognition memory, manifested as long-term habituation, requires synaptic plasticity in V1.

    Cooke, Sam F / Komorowski, Robert W / Kaplan, Eitan S / Gavornik, Jeffrey P / Bear, Mark F

    Nature neuroscience

    2015  Volume 18, Issue 6, Page(s) 926

    Language English
    Publishing date 2015-05-21
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn0615-926d
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  5. Article ; Online: Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex.

    Sidorov, Michael S / Kaplan, Eitan S / Osterweil, Emily K / Lindemann, Lothar / Bear, Mark F

    Proceedings of the National Academy of Sciences of the United States of America

    2015  Volume 112, Issue 41, Page(s) 12852–12857

    Abstract: A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). ...

    Abstract A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.
    MeSH term(s) Animals ; Dominance, Ocular/physiology ; Long-Term Synaptic Depression/physiology ; Mice ; Mice, Mutant Strains ; Receptor, Metabotropic Glutamate 5/genetics ; Receptor, Metabotropic Glutamate 5/metabolism ; Receptors, N-Methyl-D-Aspartate/genetics ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/genetics ; Synapses/metabolism ; Synaptic Transmission/physiology ; Visual Cortex/metabolism
    Chemical Substances Grm5 protein, mouse ; Receptor, Metabotropic Glutamate 5 ; Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2015-10-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1512878112
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  6. Article ; Online: Contrasting roles for parvalbumin-expressing inhibitory neurons in two forms of adult visual cortical plasticity.

    Kaplan, Eitan S / Cooke, Sam F / Komorowski, Robert W / Chubykin, Alexander A / Thomazeau, Aurore / Khibnik, Lena A / Gavornik, Jeffrey P / Bear, Mark F

    eLife

    2016  Volume 5

    Abstract: The roles played by cortical inhibitory neurons in experience-dependent plasticity are not well understood. Here we evaluate the participation of parvalbumin-expressing (PV+) GABAergic neurons in two forms of experience-dependent modification of primary ... ...

    Abstract The roles played by cortical inhibitory neurons in experience-dependent plasticity are not well understood. Here we evaluate the participation of parvalbumin-expressing (PV+) GABAergic neurons in two forms of experience-dependent modification of primary visual cortex (V1) in adult mice: ocular dominance (OD) plasticity resulting from monocular deprivation and stimulus-selective response potentiation (SRP) resulting from enriched visual experience. These two forms of plasticity are triggered by different events but lead to a similar increase in visual cortical response. Both also require the NMDA class of glutamate receptor (NMDAR). However, we find that PV+ inhibitory neurons in V1 play a critical role in the expression of SRP and its behavioral correlate of familiarity recognition, but not in the expression of OD plasticity. Furthermore, NMDARs expressed within PV+ cells, reversibly inhibited by the psychotomimetic drug ketamine, play a critical role in SRP, but not in the induction or expression of adult OD plasticity.
    MeSH term(s) Animals ; GABAergic Neurons/metabolism ; GABAergic Neurons/physiology ; Mice ; Neuronal Plasticity ; Parvalbumins/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Visual Cortex/physiology
    Chemical Substances Parvalbumins ; Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2016-03-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.11450
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  7. Article: Cell-type specific molecular signatures of aging revealed in a brain-wide transcriptomic cell-type atlas.

    Jin, Kelly / Yao, Zizhen / van Velthoven, Cindy T J / Kaplan, Eitan S / Glattfelder, Katie / Barlow, Samuel T / Boyer, Gabriella / Carey, Daniel / Casper, Tamara / Chakka, Anish Bhaswanth / Chakrabarty, Rushil / Clark, Michael / Departee, Max / Desierto, Marie / Gary, Amanda / Gloe, Jessica / Goldy, Jeff / Guilford, Nathan / Guzman, Junitta /
    Hirschstein, Daniel / Lee, Changkyu / Liang, Elizabeth / Pham, Trangthanh / Reding, Melissa / Ronellenfitch, Kara / Ruiz, Augustin / Sevigny, Josh / Shapovalova, Nadiya / Shulga, Lyudmila / Sulc, Josef / Torkelson, Amy / Tung, Herman / Levi, Boaz / Sunkin, Susan M / Dee, Nick / Esposito, Luke / Smith, Kimberly / Tasic, Bosiljka / Zeng, Hongkui

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Biological aging can be defined as a gradual loss of homeostasis across various aspects of molecular and cellular function. Aging is a complex and dynamic process which influences distinct cell types in a myriad of ways. The cellular architecture of the ... ...

    Abstract Biological aging can be defined as a gradual loss of homeostasis across various aspects of molecular and cellular function. Aging is a complex and dynamic process which influences distinct cell types in a myriad of ways. The cellular architecture of the mammalian brain is heterogeneous and diverse, making it challenging to identify precise areas and cell types of the brain that are more susceptible to aging than others. Here, we present a high-resolution single-cell RNA sequencing dataset containing ~1.2 million high-quality single-cell transcriptomic profiles of brain cells from young adult and aged mice across both sexes, including areas spanning the forebrain, midbrain, and hindbrain. We find age-associated gene expression signatures across nearly all 130+ neuronal and non-neuronal cell subclasses we identified. We detect the greatest gene expression changes in non-neuronal cell types, suggesting that different cell types in the brain vary in their susceptibility to aging. We identify specific, age-enriched clusters within specific glial, vascular, and immune cell types from both cortical and subcortical regions of the brain, and specific gene expression changes associated with cell senescence, inflammation, decrease in new myelination, and decreased vasculature integrity. We also identify genes with expression changes across multiple cell subclasses, pointing to certain mechanisms of aging that may occur across wide regions or broad cell types of the brain. Finally, we discover the greatest gene expression changes in cell types localized to the third ventricle of the hypothalamus, including tanycytes, ependymal cells, and
    Language English
    Publishing date 2023-07-27
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.07.26.550355
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  8. Article ; Online: ASCT1 (Slc1a4) transporter is a physiologic regulator of brain d-serine and neurodevelopment.

    Kaplan, Eitan / Zubedat, Salman / Radzishevsky, Inna / Valenta, Alec C / Rechnitz, Ohad / Sason, Hagit / Sajrawi, Clara / Bodner, Oded / Konno, Kohtarou / Esaki, Kayoko / Derdikman, Dori / Yoshikawa, Takeo / Watanabe, Masahiko / Kennedy, Robert T / Billard, Jean-Marie / Avital, Avi / Wolosker, Herman

    Proceedings of the National Academy of Sciences of the United States of America

    2018  Volume 115, Issue 38, Page(s) 9628–9633

    Abstract: d-serine is a physiologic coagonist of NMDA receptors, but little is known about the regulation of its synthesis and synaptic turnover. The amino acid exchangers ASCT1 (Slc1a4) and ASCT2 (Slc1a5) are candidates for regulating d-serine levels. Using ASCT1 ...

    Abstract d-serine is a physiologic coagonist of NMDA receptors, but little is known about the regulation of its synthesis and synaptic turnover. The amino acid exchangers ASCT1 (Slc1a4) and ASCT2 (Slc1a5) are candidates for regulating d-serine levels. Using ASCT1 and ASCT2 KO mice, we report that ASCT1, rather than ASCT2, is a physiologic regulator of d-serine metabolism. ASCT1 is a major d-serine uptake system in astrocytes and can also export l-serine via heteroexchange, supplying neurons with the substrate for d-serine synthesis. ASCT1-KO mice display lower levels of brain d-serine along with higher levels of l-alanine, l-threonine, and glycine. Deletion of ASCT1 was associated with neurodevelopmental alterations including lower hippocampal and striatal volumes and changes in the expression of neurodevelopmental-relevant genes. Furthermore, ASCT1-KO mice exhibited deficits in motor function, spatial learning, and affective behavior, along with changes in the relative contributions of d-serine vs. glycine in mediating NMDA receptor activity. In vivo microdialysis demonstrated lower levels of extracellular d-serine in ASCT1-KO mice, confirming altered d-serine metabolism. These alterations are reminiscent of some of the neurodevelopmental phenotypes exhibited by patients with ASCT1 mutations. ASCT1-KO mice provide a useful model for potential therapeutic interventions aimed at correcting the metabolic impairments in patients with ASCT1 mutations.
    MeSH term(s) Amino Acid Transport System ASC/genetics ; Amino Acid Transport System ASC/metabolism ; Animals ; Astrocytes/physiology ; Brain/cytology ; Brain/diagnostic imaging ; Brain/embryology ; Brain/physiology ; Cell Communication/physiology ; Disease Models, Animal ; Glycine/metabolism ; HEK293 Cells ; Humans ; Long-Term Potentiation/physiology ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microcephaly/diagnostic imaging ; Microcephaly/genetics ; Microcephaly/metabolism ; Microcephaly/pathology ; Minor Histocompatibility Antigens/genetics ; Minor Histocompatibility Antigens/metabolism ; Neurons/physiology ; Primary Cell Culture ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Serine/metabolism ; Synaptic Transmission/physiology
    Chemical Substances Amino Acid Transport System ASC ; Minor Histocompatibility Antigens ; Receptors, N-Methyl-D-Aspartate ; Slc1a4 protein, mouse ; Slc1a5 protein, mouse ; Serine (452VLY9402) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2018-09-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1722677115
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  9. Article ; Online: Early mitochondrial abnormalities in hippocampal neurons cultured from Fmr1 pre-mutation mouse model.

    Kaplan, Eitan S / Cao, Zhengyu / Hulsizer, Susan / Tassone, Flora / Berman, Robert F / Hagerman, Paul J / Pessah, Isaac N

    Journal of neurochemistry

    2012  Volume 123, Issue 4, Page(s) 613–621

    Abstract: Pre-mutation CGG repeat expansions (55-200 CGG repeats; pre-CGG) within the fragile-X mental retardation 1 (FMR1) gene cause fragile-X-associated tremor/ataxia syndrome in humans. Defects in neuronal morphology, early migration, and electrophysiological ... ...

    Abstract Pre-mutation CGG repeat expansions (55-200 CGG repeats; pre-CGG) within the fragile-X mental retardation 1 (FMR1) gene cause fragile-X-associated tremor/ataxia syndrome in humans. Defects in neuronal morphology, early migration, and electrophysiological activity have been described despite appreciable expression of fragile-X mental retardation protein (FMRP) in a pre-CGG knock-in (KI) mouse model. The triggers that initiate and promote pre-CGG neuronal dysfunction are not understood. The absence of FMRP in a Drosophila model of fragile-X syndrome was shown to increase axonal transport of mitochondria. In this study, we show that dissociated hippocampal neuronal culture from pre-CGG KI mice (average 170 CGG repeats) express 42.6% of the FMRP levels and 3.8-fold higher Fmr1 mRNA than that measured in wild-type neurons at 4 days in vitro. Pre-CGG hippocampal neurons show abnormalities in the number, mobility, and metabolic function of mitochondria at this early stage of differentiation. Pre-CGG hippocampal neurites contained significantly fewer mitochondria and greatly reduced mitochondria mobility. In addition, pre-CGG neurons had higher rates of basal oxygen consumption and proton leak. We conclude that deficits in mitochondrial trafficking and metabolic function occur despite the presence of appreciable FMRP expression and may contribute to the early pathophysiology in pre-CGG carriers and to the risk of developing clinical fragile-X-associated tremor/ataxia syndrome.
    MeSH term(s) Analysis of Variance ; Animals ; Cells, Cultured ; Fragile X Mental Retardation Protein/genetics ; Hippocampus/cytology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria/metabolism ; Mitochondria/physiology ; Neurons/metabolism ; Neurons/pathology ; Neurons/ultrastructure ; Organic Chemicals/metabolism ; Oxygen Consumption ; RNA, Messenger/metabolism ; Trinucleotide Repeat Expansion/genetics
    Chemical Substances MitoTracker Red 580 ; Organic Chemicals ; RNA, Messenger ; Fragile X Mental Retardation Protein (139135-51-6)
    Language English
    Publishing date 2012-09-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2012.07936.x
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  10. Article ; Online: Asc-1 Transporter Regulation of Synaptic Activity via the Tonic Release of d-Serine in the Forebrain.

    Sason, Hagit / Billard, Jean Marie / Smith, Garrick Paul / Safory, Hazem / Neame, Samah / Kaplan, Eitan / Rosenberg, Dina / Zubedat, Salman / Foltyn, Veronika N / Christoffersen, Claus Tornby / Bundgaard, Christoffer / Thomsen, Christian / Avital, Avi / Christensen, Kenneth Vielsted / Wolosker, Herman

    Cerebral cortex (New York, N.Y. : 1991)

    2017  Volume 27, Issue 2, Page(s) 1573–1587

    Abstract: d-Serine is a co-agonist of NMDA receptors (NMDARs) whose activity is potentially regulated by Asc-1 (SLC7A10), a transporter that displays high affinity for d-serine and glycine. Asc-1 operates as a facilitative transporter and as an antiporter, though ... ...

    Abstract d-Serine is a co-agonist of NMDA receptors (NMDARs) whose activity is potentially regulated by Asc-1 (SLC7A10), a transporter that displays high affinity for d-serine and glycine. Asc-1 operates as a facilitative transporter and as an antiporter, though the preferred direction of d-serine transport is uncertain. We developed a selective Asc-1 blocker, Lu AE00527, that blocks d-serine release mediated by all the transport modes of Asc-1 in primary cultures and neocortical slices. Furthermore, d-serine release is reduced in slices from Asc-1 knockout (KO) mice, indicating that d-serine efflux is the preferred direction of Asc-1. The selectivity of Lu AE00527 is assured by the lack of effect on slices from Asc-1-KO mice, and the lack of interaction with the co-agonist site of NMDARs. Moreover, in vivo injection of Lu AE00527 in P-glycoprotein-deficient mice recapitulates a hyperekplexia-like phenotype similar to that in Asc-1-KO mice. In slices, Lu AE00527 decreases the long-term potentiation at the Schaffer collateral-CA1 synapses, but does not affect the long-term depression. Lu AE00527 blocks NMDAR synaptic potentials when typical Asc-1 extracellular substrates are present, but it does not affect AMPAR transmission. Our data demonstrate that Asc-1 mediates tonic co-agonist release, which is required for optimal NMDAR activation and synaptic plasticity.
    Language English
    Publishing date 2017-02-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1077450-6
    ISSN 1460-2199 ; 1047-3211
    ISSN (online) 1460-2199
    ISSN 1047-3211
    DOI 10.1093/cercor/bhv350
    Database MEDical Literature Analysis and Retrieval System OnLINE

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