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Journal of Neurochemistry

Cover image for Vol. 125 Issue 5

June 2013

Volume 125, Issue 5

Pages 639–799

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATIONS
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    1. You have free access to this content
      Removing the blinkers: moving beyond striatal dopamine in Parkinson's disease (pages 639–641)

      Karen L. Eskow Jaunarajs and David G. Standaert

      Version of Record online: 20 MAY 2013 | DOI: 10.1111/jnc.12167

      Read the full article ‘Reduced noradrenaline, but not dopamine and serotonin in motor thalamus of the MPTP primate: relation to severity of Parkinsonism’ on doi: 10.1111/jnc.12162.

  2. SHORT COMMUNICATIONS

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATIONS
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    1. You have free access to this content
      Decrease of GSK3β phosphorylation in the rat nucleus accumbens core enhances cocaine-induced hyper-locomotor activity (pages 642–648)

      Wha Y. Kim, Ju K. Jang, Jung W. Lee, Hyunduk Jang and Jeong-Hoon Kim

      Version of Record online: 24 MAR 2013 | DOI: 10.1111/jnc.12222

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      The increased phosphorylation levels for GSK3β in the nucleus accumbens (NAcc) have known to attenuate psychomotor stimulants-induced hyperactivity. However, the opposite direction has not been studied. Here we found that decreased levels of GSK3β phosphorylation in the NAcc core enhance cocaine-induced hyper-locomotor activity. This is the first demonstration that the selective decrease of GSK3β phosphorylation levels actually contributes positively to cocaine-induced locomotor activity.

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      Exposure to predator odor and resulting anxiety enhances the expression of the α2δ subunit of voltage-sensitive calcium channels in the amygdala (pages 649–656)

      Carla Nasca, Rosamaria Orlando, Moreno Marchiafava, Paolo Boldrini, Giuseppe Battaglia, Sergio Scaccianoce, Francesco Matrisciano, Anna Pittaluga and Ferdinando Nicoletti

      Version of Record online: 8 JAN 2013 | DOI: 10.1111/j.1471-4159.2012.07895.x

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      Changes in α2δ subunit expression in anxiety modelThe α2δ subunit is the molecular target for pregabalin, which is used in humans for the treatment of anxiety disorders. We found that α2δ subunit was up-regulated in the amygdala in a mouse model of innate anxiety where pregabalin was proved to be effective. These findings suggest that pregabalin acts as ‘disease-dependent’ drug in the treatment of anxiety.

  3. HIGHLIGHTED ARTICLE

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATIONS
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    1. SHORT COMMUNICATIONS

      You have free access to this content
      Reduced noradrenaline, but not dopamine and serotonin in motor thalamus of the MPTP primate: relation to severity of Parkinsonism (pages 657–662)

      Christian Pifl, Oleh Hornykiewicz, Javier Blesa, Rebeca Adánez, Carmen Cavada and José A. Obeso

      Version of Record online: 13 FEB 2013 | DOI: 10.1111/jnc.12162

      Thumbnail image of graphical abstract

      Parkinson patients and animals with experimentally reduced thalamic noradrenaline exhibit pathological thalamic discharge patterns. In Parkinson's disease, motor thalamic noradrenaline is profoundly reduced. MPTP-induced parkinsonian monkeys had in addition to basal ganglia dopamine loss noradrenaline losses specifically in the motor thalamus, with the ventroanterior motor nucleus being affected only in severe parkinsonism. Thus, noradrenaline, specifically in the thalamus, appears to be an important player in the pathophysiology of Parkinson's disease.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12167.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATIONS
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Protein kinase Cβ is a modulator of the dopamine D2 autoreceptor-activated trafficking of the dopamine transporter (pages 663–672)

      Rong Chen, Conor P. Daining, Haiguo Sun, Rheaclare Fraser, Stephanie L. Stokes, Michael Leitges and Margaret E. Gnegy

      Version of Record online: 18 MAR 2013 | DOI: 10.1111/jnc.12229

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      We proposed that increased dopamine transporter membrane insertion upon activation of dopamine D2 autoreceptor is because of enhanced recycling of the transporter. This trafficking is modulated by the PKCβ - ERK signaling cascade with PKCβ upstream of ERK. Our findings suggest PKCβ as a new potential target for treatment of diseases with dysfunctional presynaptic dopaminergic transmission.

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      Intracellular Zn2+ accumulation enhances suppression of synaptic activity following spreading depolarization (pages 673–684)

      Russell E. Carter, Jessica L. Seidel, Britta E. Lindquist, Christian T. Sheline and C. William Shuttleworth

      Version of Record online: 15 APR 2013 | DOI: 10.1111/jnc.12237

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      Synaptic Zn2+ release and accumulation occurs during spreading depolarization (SD). We show here that intracellular Zn2+ accumulation significantly impairs recovery from SD, as measured by suppression of field excitatory postsynaptic potentials and DC shift durations. These effects were mediated by enhanced adenosine accumulation and A1 receptor activation. The added challenge of Zn2+ release and loading during SD may contribute to deleterious effects of Zn2+ in brain injury.

    3. Brain Development & Cell Differentiation

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      GSK-3α/β-mediated phosphorylation of CRMP-2 regulates activity-dependent dendritic growth (pages 685–697)

      Minghui Tan, Shanshan Ma, Qiaoying Huang, Kunhua Hu, Bin Song and Mingtao Li

      Version of Record online: 25 MAR 2013 | DOI: 10.1111/jnc.12230

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      Neuronal activity is critical for dendritic growth. We found that both GSK-3α and GSK-3β are involved in regulating activity-dependent dendritic growth. Neuronal activity inactivates GSK-3α/β via phosphorylation on Ser21/9, leading to the activation of their downstream effector CRMP-2, thus promoting dendritic growth. These findings identify a novel role for GSK-3/CRMP-2 pathway in connecting neuronal activity to dendritic growth.

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      Geranylgeranyltransferase I mediates BDNF-induced synaptogenesis (pages 698–712)

      Zhengwei Li, Chengdong Sun, Tao Zhang, Jianbing Mo, Qiong Shi, Xianfeng Zhang, Maochun Yuan, Long Chen, Xueqiang Mao, Rutong Yu and Xiuping Zhou

      Version of Record online: 19 APR 2013 | DOI: 10.1111/jnc.12249

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      Geranylgeranyltransferase I mediates BDNF-induced synaptogenesis

      Synaptogenesis is a complicated process of interaction between extracellular factors, such BDNF, and intracellular signaling, such as Rho family small GTPases. However, the mechanism that BDNF activated Rho family small GTPases and affected cytoskeletal reorganization and synapse formation remains unclear. In this sudy, we reported that GGT mediates BDNF-induced neuronal synaptogenesis through small GTPase Rac1 activation.

    5. Bioenergetics & Metabolism

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      Novel neuroprotective action of prothymosin alpha-derived peptide against retinal and brain ischemic damages (pages 713–723)

      Sebok Kumar Halder, Hayato Matsunaga, Haruka Yamaguchi and Hiroshi Ueda

      Version of Record online: 28 JAN 2013 | DOI: 10.1111/jnc.12132

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      This study aimed at identifying the neuroprotective domain in ProTα against ischemic stress in vitro and in vivo. The novel finding is that active peptide sequence P30 (a.a. 49–78) of ProTα ameliorates ischemia-induced cellular and functional damages. The detailed mechanisms of P30-induced neuroprotection may provide a novel solution for treatment of ischemic damages.

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      Validation of an ELISA for urinary dopamine: applications in monitoring treatment of dopamine-related disorders (pages 724–735)

      Mikaela Nichkova, Paul M. Wynveen, David T. Marc, Han Huisman and Gottfried H. Kellermann

      Version of Record online: 25 APR 2013 | DOI: 10.1111/jnc.12248

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      Our competitive ELISA for direct dopamine quantification in urine samples is a viable cost-effective alternative to chromatographic analysis. The method is robust, sensitive, and very specific and it does not require sample pre-treatment. It can be used in monitoring dopamine-modulating therapies. Urinary dopamine levels significantly increase in a dose-dependent manner for Parkinson's disease patients under l-DOPA treatment.

    7. Neuronal Plasticity & Behaviour

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      Memory impairment and hippocampus specific protein oxidation induced by ethanol intake and 3, 4-Methylenedioxymethamphetamine (MDMA) in mice (pages 736–746)

      Clara Ros-Simó, Maria Moscoso-Castro, Jéssica Ruiz-Medina, Joaquim Ros and Olga Valverde

      Version of Record online: 22 APR 2013 | DOI: 10.1111/jnc.12247

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      Ethanol and MDMA are two commonly co-abused drugs among adolescents with detrimental side effects. Oxidative stress is induced by these drugs of abuse and can damage specific proteins and affect important cellular functions in brains of consumers. Our findings reveal that specific hippocampus proteins are oxidatively damaged and memory processes are affected. Our findings reveal that specific hippocampus proteins are oxidatively damaged after ethanol and MDMA administration and memory processes are affected.

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      Involvement of the K+-Cl co-transporter KCC2 in the sensitization to morphine-induced hyperlocomotion under chronic treatment with zolpidem in the mesolimbic system (pages 747–755)

      Masahiro Shibasaki, Daiki Masukawa, Kazunori Ishii, Yui Yamagishi, Tomohisa Mori and Tsutomu Suzuki

      Version of Record online: 25 APR 2013 | DOI: 10.1111/jnc.12258

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      We found that chronic treatment with benzodiazepines enhanced morphine-induced hyperlocomotion through the increase of KCC2 in the nucleus accumbens. Furthermore, phosphorylation of protein kinase C γ (PKCγ induced the up-regulation of KCC2 through inactivation of protein phosphatase-1 (PP-1). These findings indicate that chronic treatment with benzodiazepines enhances dopaminergic signal transduction as a post-synaptic event.

    9. Neuroinfl ammation & Neuroimmunology

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      The role of MAC1 in diesel exhaust particle-induced microglial activation and loss of dopaminergic neuron function (pages 756–765)

      Shannon Levesque, Thomas Taetzsch, Melinda E. Lull, Jo Anne Johnson, Constance McGraw and Michelle L. Block

      Version of Record online: 2 APR 2013 | DOI: 10.1111/jnc.12231

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      Diesel exhaust particles (DEP) are a major component of urban air pollution, which has been linked to microglial activation and Parkinson's disease-like pathology. Urban particulate matter is reported to reach the brain, but how microglia identify and respond to DEP is poorly understood. These findings reveal that pattern recognition receptors are key to the microglial response to DEP, where scavenger receptors regulate the internalization and MAC1 mediates ROS production and loss of DA neuron function.

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      Progression in multiple sclerosis is associated with low endogenous NCAM (pages 766–773)

      Sharmilee Gnanapavan, Peggy Ho, Wendy Heywood, Sam Jackson, Donna Grant, Khadija Rantell, Geoff Keir, Kevin Mills, Lawrence Steinman and Gavin Giovannoni

      Version of Record online: 19 APR 2013 | DOI: 10.1111/jnc.12236

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      We provide in-vitro and in-vivo evidence that NCAM is adversely affected by demyelination and is steadily depleted through CIS, RRMS and SPMS. We think that reduction in NCAM is one of the factors associated with or possibly responsible for the progression of MS.

    11. Molecular Basis of Disease

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      Characterization of electroencephalographic and biochemical responses at 5-HT promoting drug-induced onset of serotonin syndrome in rats (pages 774–789)

      Zhiyuan Ma, Mary Rudacille, Howard M. Prentice and Rui Tao

      Version of Record online: 28 JAN 2013 | DOI: 10.1111/jnc.12141

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      Serotonin (5HT) is known to improve mood, however, only when the levels of its release are in an appropriate range. Excessive 5HT is harmful, likely resulting in serotonin syndrome. The present study was to characterize the syndrome, suggesting that the syndrome onset can be revealed with EEG, measurements of tremor activity and changes of unbound 5HT concentration in the plasma.

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      Zyxin is a novel target for beta-amyloid peptide: characterization of its role in Alzheimer's pathogenesis (pages 790–799)

      Cristina Lanni, Daniela Necchi, Antonella Pinto, Erica Buoso, Laura Buizza, Maurizio Memo, Daniela Uberti, Stefano Govoni and Marco Racchi

      Version of Record online: 13 FEB 2013 | DOI: 10.1111/jnc.12154

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      Putative role of zyxin in Alzheimer pathogenesis Soluble Aβ modulates zyxin protein levels, fundamental in maintaining HIPK2 stability and p53 activity. When zyxin is down-regulated by Aβ peptides, HIPK2 activity is inhibited, thus inducing an altered conformational state of p53. These results may help the studies on Alzheimer pathogenesis, through the fine dissection of events related to Aβ activities.

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