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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
    Linköpings universitet, Institutionen för fysik, kemi och biologi. Linköpings universitet, Tekniska högskolan.
    Regulators acting in combinatorial codes also act independently in single differentiating neurons2005Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 45, nr 5, s. 689-700Artikel i tidskrift (Refereegranskat)
    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.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Heilig, Markus
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Psykiatriska kliniken.
    mTORC and ProSAPiP1: How Alcohol Changes Synapses of Reward Circuitry2017Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 96, nr 1Artikel i tidskrift (Övrigt vetenskapligt)
    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.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Large-Scale Movement within the Voltage-Sensor Paddle of a Potassium Channel-Support for a Helical-Screw Motion2008Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 59, nr 5, s. 770-777Artikel i tidskrift (Refereegranskat)
    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 seeking2008Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 59, nr 3, s. 497-508Artikel i tidskrift (Refereegranskat)
    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.
    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 synapses2006Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 51, nr 6, s. 773-786Artikel i tidskrift (Refereegranskat)
    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.

  • 6.
    Larsson, HP
    et al.
    Karolinska Institute.
    Elinder, Fredrik
    Karolinska Institute.
    A conserved glutamate is important for slow inactivation in K+ channels2000Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 27, nr 3, s. 573-583Artikel i tidskrift (Refereegranskat)
    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.

  • 7.
    McGlone, Francis
    et al.
    Liverpool John Moores University, England University of Liverpool, England .
    Wessberg, Johan
    University of Gothenburg, Sweden .
    Olausson, Håkan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Neurofysiologiska kliniken US.
    Discriminative and Affective Touch: Sensing and Feeling2014Ingår i: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 82, nr 4, s. 737-755Artikel, forskningsöversikt (Refereegranskat)
    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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