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Neuron 27건

  1. [해외논문]   Autoantibodies Hurt: Transfer of Patient-Derived CASPR2 Antibodies Induces Neuropathic Pain in Mice   SCI SCIE

    Hunt, Matthew A. (Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Nascimento, Diana S.M. (Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Bersellini Farinotti, Alex (Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden ) , Svensson, Camilla I. (Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden)
    Neuron v.97 no.4 ,pp. 729 - 731 , 2018 , 0896-6273 ,

    초록

    In this issue of Neuron , show that CASPR2 antibodies (Abs) isolated from patients bind specifically to primary afferent cell bodies and induce neuropathic pain in mice. Consequent decreased expression of Kv1 channels and their aberrant localization along myelinated axons explain the observed hyperexcitability and pain.

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  2. [해외논문]   Everything in Its Right Place: A Prefrontal-Midbrain Circuit for Contextual Fear Discrimination   SCI SCIE

    Bukalo, Olena (Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA ) , Holmes, Andrew (Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA)
    Neuron v.97 no.4 ,pp. 732 - 733 , 2018 , 0896-6273 ,

    초록

    In this issue of Neuron , use an ingenuous behavioral paradigm to change pertinent sensory stimuli defining a given context to interrogate how the dorsomedial prefrontal cortex (dmPFC) and periaqueductal gray (PAG) interact during contextual fear discrimination.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   Causal Evidence for a Neural Component of Spatially Global Hemodynamic Signals   SCI SCIE

    Mü (Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA ) , sch, Kathrin (Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA) , Honey, Christopher J.
    Neuron v.97 no.4 ,pp. 734 - 736 , 2018 , 0896-6273 ,

    초록

    In this issue of Neuron , reversibly inactivate the basal forebrain to show that this region magnifies global neocortical signal fluctuations without altering the topography of canonical resting-state networks. Thus, spatially diffuse signals measurable via functional neuroimaging may track large-scale neuromodulatory state changes in the primate brain.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  4. [해외논문]   Untangling Neural Representations in the Motor Cortex   SCI SCIE

    Jackson, Andrew (Institute of Neuroscience, Newcastle University, Newcastle NE2 1HP, UK)
    Neuron v.97 no.4 ,pp. 736 - 738 , 2018 , 0896-6273 ,

    초록

    How the brain generates accurate movement is a long-standing problem in neuroscience. In this issue of Neuron , argue that population activity in motor cortex does not represent muscle patterns but rather untangled neural trajectories that are robust to noise.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  5. [해외논문]   A Spotlight on Appetite   SCI SCIE

    Beutler, Lisa R. (Department of Medicine, University of California, San Francisco, San Francisco, CA 94158, USA ) , Knight, Zachary A. (Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA)
    Neuron v.97 no.4 ,pp. 739 - 741 , 2018 , 0896-6273 ,

    초록

    Remarkably few hormones have been identified that stimulate appetite. The recent discovery of asprosin, a hormone that activates AgRP neurons to increase food intake and body weight, begins to fill this gap ().

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Multiple Sclerosis: Mechanisms and Immunotherapy   SCI SCIE

    Baecher-Allan, Clare (Department of Neurology, Ann Romney Center for Neurologic Diseases, Partners MS Center, Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA ) , Kaskow, Belinda J. (Department of Neurology, Ann Romney Center for Neurologic Diseases, Partners MS Center, Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA ) , Weiner, Howard L. (Department of Neurology, Ann Romney Center for Neurologic Diseases, Partners MS Center, Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA)
    Neuron v.97 no.4 ,pp. 742 - 768 , 2018 , 0896-6273 ,

    초록

    Multiple sclerosis (MS) is an autoimmune disease triggered by environmental factors that act on a genetically susceptible host. It features three clinical stages: a pre-clinical stage detectable only by MRI; a relapsing-remitting (RRMS) stage characterized by episodes of neurologic dysfunction followed by resolution; and a progressive stage, which usually evolves from the relapsing stage. Advances in our understanding of the immune mechanisms that contribute to MS have led to more than ten FDA-approved immunotherapeutic drugs that target effector T cells, regulatory cells, B cells, and cell trafficking into the nervous system. However, most drugs for relapsing MS are not effective in treating progressive disease. Progressive MS features a compartmentalized immune response in the central nervous system, involving microglia cells and astrocytes, as well as immune-independent processes that drive axonal dysfunction. Major challenges for MS research involve understanding the mechanisms of disease progression, developing treatment for progressive MS, and determining the degree to which progressive disease can be prevented by early treatment. Key priorities for MS research include developing biomarkers, personalized medicine and advanced imaging, and a better understanding of the microbiome. With a better understanding of the genetic and epidemiological aspects of this disease, approaches to prevent MS are now also being considered.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Neuromodulation of Attention   SCI SCIE

    Thiele, Alexander (Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK ) , Bellgrove, Mark A. (Monash Institute of Cognitive and Clinical Neurosciences (MICCN) and School of Psychological Sciences, Monash University, Melbourne, Australia)
    Neuron v.97 no.4 ,pp. 769 - 785 , 2018 , 0896-6273 ,

    초록

    Attention is critical to high-level cognition and attention deficits are a hallmark of neurologic and neuropsychiatric disorders. Although years of research indicates that distinct neuromodulators influence attentional control, a mechanistic account that traverses levels of analysis (cells, circuits, behavior) is missing. However, such an account is critical to guide the development of next-generation pharmacotherapies aimed at forestalling or remediating the global burden associated with disorders of attention. Here, we summarize current neuroscientific understanding of how attention affects single neurons and networks of neurons. We then review key results that have informed our understanding of how neuromodulation shapes these neuron and network properties and thereby enables the appropriate allocation of attention to relevant external or internal events. Finally, we highlight areas where we believe hypotheses can be formulated and tackled experimentally in the near future, thereby critically increasing our mechanistic understanding of how attention is implemented at the cellular and network levels.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [해외논문]   A Subpopulation of Striatal Neurons Mediates Levodopa-Induced Dyskinesia   SCI SCIE

    Girasole, Allison E. (Neuroscience Graduate Program, UCSF, San Francisco, CA 94158, USA ) , Lum, Matthew Y. (Department of Neurology, UCSF, San Francisco, CA 94158, USA ) , Nathaniel, Diane (Department of Neurology, UCSF, San Francisco, CA 94158, USA ) , Bair-Marshall, Chloe J. (Department of Neurology, UCSF, San Francisco, CA 94158, USA ) , Guenthner, Casey J. (Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA ) , Luo, Liqun (Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA ) , Kreitzer, Anatol C. (Neuroscience Graduate Program, UCSF, San Francisco, CA 94158, USA ) , Nelson, Alexandra B. (Neuroscience Graduate Program, UCSF, San Francisco, CA 94158, USA)
    Neuron v.97 no.4 ,pp. 787 - 795.e6 , 2018 , 0896-6273 ,

    초록

    Summary Parkinson’s disease is characterized by the progressive loss of midbrain dopamine neurons. Dopamine replacement therapy with levodopa alleviates parkinsonian motor symptoms but is complicated by the development of involuntary movements, termed levodopa-induced dyskinesia (LID). Aberrant activity in the striatum has been hypothesized to cause LID. Here, to establish a direct link between striatal activity and dyskinesia, we combine optogenetics and a method to manipulate dyskinesia-associated neurons, targeted recombination in active populations (TRAP). We find that TRAPed cells are a stable subset of sensorimotor striatal neurons, predominantly from the direct pathway, and that reactivation of TRAPed striatal neurons causes dyskinesia in the absence of levodopa. Inhibition of TRAPed cells, but not a nonspecific subset of direct pathway neurons, ameliorates LID. These results establish that a distinct subset of striatal neurons is causally involved in LID and indicate that successful therapeutic strategies for treating LID may require targeting functionally selective neuronal subtypes. Highlights FosTRAP captures neurons activated in levodopa-induced dyskinesia (LID) brain-wide Primarily striatal direct pathway neurons (dMSNs) are activated during dyskinesia Reactivation of TRAPed striatal neurons produces dyskinesia in the absence of levodopa Inhibition of TRAPed striatal neurons, but not nonspecific dMSNs, reduces LID

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   Retrograde Signaling from Progranulin to Sort1 Counteracts Synapse Elimination in the Developing Cerebellum  

    Uesaka, Naofumi , Abe, Manabu , Konno, Kohtarou , Yamazaki, Maya , Sakoori, Kazuto , Watanabe, Takaki , Kao, Tzu-Huei , Mikuni, Takayasu , Watanabe, Masahiko , Sakimura, Kenji , Kano, Masanobu
    Neuron v.97 no.4 ,pp. 796 - 805.e5 , 2018 , 0896-6273 ,

    초록

    Summary Parkinson’s disease is characterized by the progressive loss of midbrain dopamine neurons. Dopamine replacement therapy with levodopa alleviates parkinsonian motor symptoms but is complicated by the development of involuntary movements, termed levodopa-induced dyskinesia (LID). Aberrant activity in the striatum has been hypothesized to cause LID. Here, to establish a direct link between striatal activity and dyskinesia, we combine optogenetics and a method to manipulate dyskinesia-associated neurons, targeted recombination in active populations (TRAP). We find that TRAPed cells are a stable subset of sensorimotor striatal neurons, predominantly from the direct pathway, and that reactivation of TRAPed striatal neurons causes dyskinesia in the absence of levodopa. Inhibition of TRAPed cells, but not a nonspecific subset of direct pathway neurons, ameliorates LID. These results establish that a distinct subset of striatal neurons is causally involved in LID and indicate that successful therapeutic strategies for treating LID may require targeting functionally selective neuronal subtypes. Highlights FosTRAP captures neurons activated in levodopa-induced dyskinesia (LID) brain-wide Primarily striatal direct pathway neurons (dMSNs) are activated during dyskinesia Reactivation of TRAPed striatal neurons produces dyskinesia in the absence of levodopa Inhibition of TRAPed striatal neurons, but not nonspecific dMSNs, reduces LID

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    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  10. [해외논문]   Retrograde Signaling from Progranulin to Sort1 Counteracts Synapse Elimination in the Developing Cerebellum   SCI SCIE

    Uesaka, Naofumi (Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan ) , Abe, Manabu (Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan ) , Konno, Kohtarou (Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan ) , Yamazaki, Maya (Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan ) , Sakoori, Kazuto (Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan ) , Watanabe, Takaki (Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan ) , Kao, Tzu-Huei (Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan ) , Mikuni, Takayasu (Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan ) , Watanabe, Masahiko (Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan ) , Sakimura, Kenji (Department of Cellular Neurobiology, Brai) , Kano, Masanobu
    Neuron v.97 no.4 ,pp. 796 - 805.e5 , 2018 , 0896-6273 ,

    초록

    Summary Elimination of redundant synapses formed early in development and strengthening of necessary connections are crucial for shaping functional neural circuits. Purkinje cells (PCs) in the neonatal cerebellum are innervated by multiple climbing fibers (CFs) with similar strengths. A single CF is strengthened whereas the other CFs are eliminated in each PC during postnatal development. The underlying mechanisms, particularly for the strengthening of single CFs, are poorly understood. Here we report that progranulin, a multi-functional growth factor implicated in the pathogenesis of frontotemporal dementia, strengthens developing CF synaptic inputs and counteracts their elimination from postnatal day 11 to 16. Progranulin derived from PCs acts retrogradely onto its putative receptor Sort1 on CFs. This effect is independent of semaphorin 3A, another retrograde signaling molecule that counteracts CF synapse elimination. We propose that progranulin-Sort1 signaling strengthens and maintains developing CF inputs, and may contribute to selection of single “winner” CFs that survive synapse elimination. Highlights Progranulin is a PC-derived regulator of developmental CF synapse elimination Progranulin from PCs counteracts synapse elimination and reinforces the strongest CF Progranulin acts on developing CF synapses from P11 to P16 independently of Sema3A Sort1 on CFs mediates the retrograde action of progranulin on CF synapse elimination

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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