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  • 1.
    Allan, D.W.
    et al.
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, United States, Department of Neurology, 211 Enders, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, United States.
    Park, D.
    Dept. of Anatomy and Neurobiology, Washington University, School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, United States.
    St., Pierre S.E.
    St. Pierre, S.E., Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, United States, Cutaneous Biology Research Center, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, United States.
    Taghert, P.H.
    Dept. of Anatomy and Neurobiology, Washington University, School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, United States.
    Thor, Stefan
    Linköping University, Department of Physics, Chemistry and Biology. Linköping University, The Institute of Technology.
    Regulators acting in combinatorial codes also act independently in single differentiating neurons2005In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 45, no 5, p. 689-700Article in journal (Refereed)
    Abstract [en]

    In the Drosophila ventral nerve cord, a small number of neurons express the LIM-homeodomain gene apterous (ap). These ap neurons can be subdivided based upon axon pathfinding and their expression of neuropeptidergic markers. ap, the zinc finger gene squeeze, the bHLH gene dimmed, and the BMP pathway are all required for proper specification of these cells. Here, using several ap neuron terminal differentiation markers, we have resolved how each of these factors contributes to ap neuron diversity. We find that these factors interact genetically and biochemically in subtype-specific combinatorial codes to determine certain defining aspects of ap neuron subtype identity. However, we also find that ap, dimmed, and squeeze additionally act independently of one another to specify certain other defining aspects of ap neuron subtype identity. Therefore, within single neurons, we show that single regulators acting in numerous molecular contexts differentially specify multiple subtype-specific traits. Copyright ©2005 by Elsevier Inc.

  • 2.
    Barbier, Estelle
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Heilig, Markus
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Local Health Care Services in Central Östergötland, Department of Psychiatry.
    mTORC and ProSAPiP1: How Alcohol Changes Synapses of Reward Circuitry2017In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 96, no 1Article in journal (Other academic)
    Abstract [en]

    Alcohol addiction is characterized by broad and persistent changes in brain function, but the underlying neural adaptations remain largely unknown. In this issue of Neuron, Laguesse et al. (2017) describe a neural mechanism through which long-term alcohol exposure induces structural and synaptic adaptations that promote excessive alcohol use.

  • 3.
    Broomand, Amir
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Elinder, Fredrik
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Large-Scale Movement within the Voltage-Sensor Paddle of a Potassium Channel-Support for a Helical-Screw Motion2008In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 59, no 5, p. 770-777Article in journal (Refereed)
    Abstract [en]

    The size of the movement and the molecular identity of the moving parts of the voltage sensor of a voltage-gated ion channel are debated. In the helical-screw model, the positively charged fourth transmembrane segment S4 slides and rotates along negative counter charges in S2 and S3, while in the paddle model, S4 carries the extracellular part of S3 (S3b) as a cargo. Here, we show that S4 slides 16-26 Å along S3b. We introduced pairs of cysteines in S4 and S3b of the Shaker K channel to make disulfide bonds. Residue 325 in S3b makes close and state-dependent contacts with a long stretch of residues in S4. A disulfide bond between 325 and 360 was formed in the closed state, while a bond between 325 and 366 was formed in the open state. These data are not compatible with the voltage-sensor paddle model, but support the helical-screw model. © 2008 Elsevier Inc. All rights reserved.

  • 4.
    Engblom, David
    et al.
    German Cancer Research Center, Heidelberg.
    Bilbao, Ainhoa
    Central Institute of Mental Health, Mannheim.
    Sanchis-Segura, Carles
    Central Institute of Mental Health, Mannheim.
    Dahan, Lionel
    University of Geneva.
    Perreau-Lenz, Stephanie
    Central Institute of Mental Health, Mannheim.
    Balland, Benedicte
    University of Geneva.
    Rodriguez Parkitna, Jan
    German Cancer Research Center, Heidelberg.
    Lujan, Rafael
    University of Castilla La Mancha.
    Halbout, Briac
    Central Institute of Mental Health, Mannheim.
    Mameli, Manuel
    University of Geneva.
    Parlato, Rosanna
    German Cancer Research Center, Heidelberg.
    Sprengel, Rolf
    Max Planck Institute.
    Luescher, Christian
    University of Geneva.
    Schuetz, Guenther
    German Cancer Research Center, Heidelberg.
    Spanagel, Rainer
    Central Institute of Mental Health, Mannheim.
    Glutamate receptors on dopamine neurons control the persistence of cocaine seeking2008In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 59, no 3, p. 497-508Article in journal (Refereed)
    Abstract [en]

    Cocaine strengthens excitatory synapses onto midbrain dopamine neurons through the synaptic delivery of GluR1-containing AMPA receptors. This cocaine-evoked plasticity depends on NMDA receptor activation, but its behavioral significance in the context of addiction remains elusive. Here, we generated mice lacking the GluR1, GluR2, or NR1 receptor subunits selectively in dopamine neurons. We report that in midbrain slices of cocaine-treated mice, synaptic transmission was no longer strengthened when GluR1 or NR1 was abolished, while in the respective mice the drug still induced normal conditioned place preference and locomotor sensitization. In contrast, extinction of drug-seeking behavior was absent in mice lacking GluR1, while in the NR1 mutant mice reinstatement was abolished. In conclusion, cocaine-evoked synaptic plasticity does not mediate concurrent short-term behavioral effects of the drug but may initiate adaptive changes eventually leading to the persistence of drug-seeking behavior.

  • 5.
    Gau, Rémi
    et al.
    Institute of Psychology, Université Catholique de Louvain, Louvain la Neuve, Belgium. Electronic address remi.gau@uclouvain.be.
    Noble, Stephanie
    Radiology & Biomedical Imaging, Yale University, New Haven CT, USA.
    Heuer, Katja
    Center for Research and Interdisciplinarity, Université of Paris, Paris, France; Department of Neuropsychology, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
    Bottenhorn, Katherine L
    Department of Psychology, Florida International University, Miami, FL, USA.
    Bilgin, Isil P
    Biomedical Engineering, Cybernetics, University of Reading, Reading, UK; Allied Health Professions Institute, University of the West of England, Bristol, UK.
    Yang, Yu-Fang
    Department of Psychology, University of Würzburg, Würzburg, Germany.
    Huntenburg, Julia M
    Systems Neuroscience Lab, Champalimaud Research, Lisbon, Portugal.
    Bayer, Johanna M M
    Centre for Youth Mental Health, University of Melbourne, Melbourne, Australia; Orygen Youth Health, Melbourne, Australia.
    Bethlehem, Richard A I
    Autism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, UK; Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Cambridge, UK.
    Rhoads, Shawn A
    Department of Psychology, Georgetown University, Washington DC, USA.
    Vogelbacher, Christoph
    Laboratory for Multimodal Neuroimaging, Department of Psychiatry and Psychotherapy, University of Marburg, Marburg, Germany.
    Borghesani, Valentina
    Centre de Recherche de lInstitut Universitaire de Gériatrie de Montréal, Université de Montréal, Montréal, QC, Canada.
    Levitis, Elizabeth
    Section on Developmental Neurogenomics, National Institute of Mental Health, Bethesda, MD, USA; Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK.
    Wang, Hao-Ting
    Sackler Centre for Consciousness Science, University of Sussex, Brighton, UK; Department of Neuroscience, Brighton and Sussex Medical School, University of Sussex, Brighton, UK; Sussex Neuroscience, University of Sussex, Brighton, UK.
    Van Den Bossche, Sofie
    Department of Data Analysis, Faculty of Psychology and Educational Sciences, Ghent University, Ghent, Belgium.
    Kobeleva, Xenia
    Department of Neurology, University of Bonn, Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
    Legarreta, Jon Haitz
    Computer Science, Université de Sherbrooke, Sherbrooke, QC, Canada.
    Guay, Samuel
    Université de Montréal, Montréal, QC, Canada.
    Atay, Selim Melvin
    Neuroscience and Neurotechnology, Middle East Technical University, Ankara, Turkey.
    Varoquaux, Gael P
    Parietal, INRIA, Saclay, France; Montréal Neurological Institute, McGill University, Montréal, QC, Canada.
    Huijser, Dorien C
    Erasmus School of Social and Behavioural Sciences, Erasmus University Rotterdam, Rotterdam, the Netherlands; Developmental and Educational Psychology, Leiden University, Leiden, the Netherlands.
    Sandström, Malin S
    INCF, Karolinska Institute, Stockholm, Sweden.
    Herholz, Peer
    NeuroDataScience - ORIGAMI laboratory, Faculty of Medicine and Health Sciences McGill University Montréal, QC Canada.
    Nastase, Samuel A
    Princeton Neuroscience Institute, Princeton University, Princeton, NJ, USA.
    Badhwar, AmanPreet
    Centre de Recherche de lInstitut Universitaire de Gériatrie de Montréal, Université de Montréal, Montréal, QC, Canada; Multiomics Investigation of Neurodegenerative Diseases (MIND) Lab, Université de Montréal, Montréal, QC, Canada; Département de Pharmacologie et Physiologie, Université de Montréal, Montréal, QC, Canada.
    Dumas, Guillaume
    Department of Psychiatry, Université de Montréal, Montréal, QC, Canada; Mila, Université de Montréal, Montréal, QC, Canada.
    Schwab, Simon
    Department of Biostatistics & Center for Reproducible Research, University of Zurich, Zurich, Switzerland.
    Moia, Stefano
    Basque Center on Cognition, Brain and Language, San Sebastián-Donostia, Spain; University of the Basque Country (EHU UPV), San Sebastián-Donostia, Spain.
    Dayan, Michael
    Human Neuroscience Platform, Fondation Campus Biotech Geneva, Geneva, Switzerland.
    Bassil, Yasmine
    Graduate Division of Biological & Biomedical Sciences, Emory University, Atlanta, GA, USA.
    Brooks, Paula P
    Princeton Neuroscience Institute, Princeton University, Princeton, NJ, USA.
    Mancini, Matteo
    Department of Neuroscience, Brighton and Sussex Medical School, University of Sussex, Brighton, UK; Cardiff University Brain Research Imaging Centre, Cardiff University, Cardiff, UK; NeuroPoly Lab, Polytechnique Montréal, Montréal, QC, Canada.
    Shine, James M
    Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
    OConnor, David
    Department of Biomedical Engineering, Yale University, New Haven, CT, USA.
    Xie, Xihe
    Department of Neuroscience, Weill Cornell Medicine, New York City, NY, USA.
    Poggiali, Davide
    Padova Neuroscience Center, University of Padova, Padova, Italy.
    Friedrich, Patrick
    Institute of Neuroscience and Medicine, Brain & Behaviour (INM-7), Research Centre Jülich, Jülich, Germany.
    Heinsfeld, Anibal S
    Computational Neuroimaging Lab, University of Texas at Austin, Austin, TX, USA; Department of Computer Science, University of Texas at Austin, Austin, TX, USA.
    Riedl, Lydia
    Department of Psychiatry and Psychotherapy, Philipps Universität, Marburg, Germany.
    Toro, Roberto
    Center for Research and Interdisciplinarity, Université of Paris, Paris, France; Neuroscience Department, Institut Pasteur, Paris, France.
    Caballero-Gaudes, César
    Basque Center on Cognition, Brain and Language, San Sebastián-Donostia, Spain.
    Eklund, Anders
    Linköping University, Department of Biomedical Engineering, Division of Biomedical Engineering. Linköping University, Department of Computer and Information Science, The Division of Statistics and Machine Learning. Linköping University, Faculty of Science & Engineering. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Garner, Kelly G
    Queensland Brain Institute, The University of Queensland, St Lucia, Australia; School of Psychology, University of Birmingham, Birmingham, UK; School of Psychology, The University of Queensland, St Lucia, Australia.
    Nolan, Christopher R
    School of Psychology, University of New South Wales, Sydney, Australia.
    Demeter, Damion V
    Psychology Department, The University of Texas at Austin, Austin, TX, USA.
    Barrios, Fernando A
    Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.
    Merchant, Junaid S
    Neuroscience and Cognitive Science Program, University of Maryland, College Park, MD, USA; Department of Psychology, University of Maryland, College Park, MD, USA.
    McDevitt, Elizabeth A
    Princeton Neuroscience Institute, Princeton University, Princeton, NJ, USA.
    Oostenveld, Robert
    Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands; NatMEG, Karolinska Institutet, Stockholm, Sweden.
    Craddock, R Cameron
    Department of Diagnostic Medicine, The University of Texas at Austin Dell Medical School, Austin, TX, USA.
    Rokem, Ariel
    Psychology and eScience Institute, University of Washington, Seattle, WA, USA.
    Doyle, Andrew
    McGill Centre for Integrative Neuroscience, McGill University, Montréal, QC, Canada.
    Ghosh, Satrajit S
    McGovern Institute for Brain Research, MIT, Cambridge, MA, USA; Department of Otolaryngology - Head and Neck Surgery, Harvard Medical School, Boston, MA, USA.
    Nikolaidis, Aki
    Center for the Developing Brain, Child Mind Institute, New York City, NY, USA.
    Stanley, Olivia W
    Centre for Functional and Metabolic Mapping, University of Western Ontario, London, ON, Canada; Department of Medical Biophysics, University of Western Ontario, London, ON, Canada.
    Uruñuela, Eneko
    Basque Center on Cognition, Brain and Language, San Sebastián-Donostia, Spain; University of the Basque Country (EHU UPV), San Sebastián-Donostia, Spain.
    Brainhack: Developing a culture of open, inclusive, community-driven neuroscience2021In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 109, no 11, p. 1769-1775Article in journal (Refereed)
    Abstract [en]

    Brainhack is an innovative meeting format that promotes scientific collaboration and education in an open, inclusive environment. This NeuroView describes the myriad benefits for participants and the research community and how Brainhacks complement conventional formats to augment scientific progress.

    Download full text (pdf)
    fulltext
  • 6.
    Granseth, Björn
    et al.
    MRC Laboratory of Molecular Biology, Cambridge.
    Odermatt, Benjamin
    MRC-LMB, Cambridge.
    Royle, Stephen J
    MRC-LMB, Cambridge.
    Lagnado, Leon
    MRC-LMB, Cambridge.
    Clathrin-mediated endocytosis is the dominant mechanism of vesicle retrieval at hippocampal synapses2006In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 51, no 6, p. 773-786Article in journal (Refereed)
    Abstract [en]

    The maintenance of synaptic transmission requires that vesicles be recycled after releasing neurotransmitter. Several modes of retrieval have been proposed to operate at small synaptic terminals of central neurons, including a fast "kiss-and-run" mechanism that releases neurotransmitter through a fusion pore. Using an improved fluorescent reporter comprising pHluorin fused to synaptophysin, we find that only a slow mode of endocytosis (tau = 15 s) operates at hippocampal synapses when vesicle fusion is triggered by a single nerve impulse or short burst. This retrieval mechanism is blocked by overexpression of the C-terminal fragment of AP180 or by knockdown of clathrin using RNAi, and it is associated with the movement of clathrin and vesicle proteins out of the synapse. These results indicate that clathrin-mediated endocytosis is the major, if not exclusive, mechanism of vesicle retrieval after physiological stimuli.

  • 7.
    Heilig, Markus
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Psykiatricentrum, Psykiatriska kliniken i Linköping.
    Barbier, Estelle
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Cycles of addiction and loneliness2022In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 110, no 24, p. 4035-4037Article in journal (Other academic)
    Abstract [en]

    In this issue of Neuron, Pomrenze and colleagues(1) report a novel mechanism behind sociability deficits in mice during protracted withdrawal from morphine. Dorsal raphe dynorphin neurons terminating in the nucleus accumbens suppress local serotonin release through kappa opioid receptors. These findings likely have important clinical implications.

  • 8.
    Larsson, HP
    et al.
    Karolinska Institute.
    Elinder, Fredrik
    Karolinska Institute.
    A conserved glutamate is important for slow inactivation in K+ channels2000In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 27, no 3, p. 573-583Article in journal (Refereed)
    Abstract [en]

    Voltage-gated ion channels undergo slow inactivation during prolonged depolarizations. We investigated the role of a conserved glutamate at the extracellular end of segment 5 (S5) in slow inactivation by mutating it to a cysteine (E418C in Shaker). We could lock the channel in two different conformations by disulfide-linking 418C to two different cysteines, introduced in the Pore-S6 (P-S6) loop. Our results suggest that E418 is normally stabilizing the open conformation of the slow inactivation gate by forming hydrogen bonds with the P-S6 loop. Breaking these bonds allows the P-S6 loop to rotate, which closes the slow inactivation gate. Our results also suggest a mechanism of how the movement of the voltage sensor can induce slow inactivation by destabilizing these bonds.

  • 9.
    McGlone, Francis
    et al.
    Liverpool John Moores University, England University of Liverpool, England .
    Wessberg, Johan
    University of Gothenburg, Sweden .
    Olausson, Håkan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Department of Clinical Neurophysiology.
    Discriminative and Affective Touch: Sensing and Feeling2014In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 82, no 4, p. 737-755Article, review/survey (Refereed)
    Abstract [en]

    The multimodal properties of the human somatosensory system continue to be unravelled. There is mounting evidence that one of these submodalities-touch-has another dimension, providing not only its well-recognized discriminative input to the brain, but also an affective input. It has long been recognized that touch plays an important role in many forms of social communication and a number of theories have been proposed to explain observations and beliefs about the "power of touch." Here, we propose that a class of low-threshold mechanosensitive C fibers that innervate the hairy skin represent the neurobiological substrate for the affective and rewarding properties of touch.

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