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Journal of Neurochemistry

Cover image for Vol. 129 Issue 5

June 2014

Volume 129, Issue 5

Pages i–viii, 753–894

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
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      Issue Cover (June 2014)

      Version of Record online: 18 MAY 2014 | DOI: 10.1111/jnc.12561

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      Front cover: Image of primary hippocampal neurons immunostained with E2F1 (Green), PSD-95 (Red), and MAP2 (Blue). J. Neurochem. 2014, vol. 129 (5), pp. 850–863.

      Read the full article on doi: 10.1111/jnc.12655

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
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      Issue Information (pages i–ii)

      Version of Record online: 18 MAY 2014 | DOI: 10.1111/jnc.12562

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
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  4. EDITORIAL HIGHLIGHT

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
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      A role for SNAREs in neuronal survival? (pages 753–755)

      Callista B. Harper, Adekunle T. Bademosi, Elizabeth J. Coulson and Frederic A. Meunier

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12699

      Read the full article ‘Botulinum protease-cleaved snare fragments induce cytotoxicity in neuroblastoma cells’ on page 781.

  5. REVIEW ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
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      Insights into the physiological function of the β-amyloid precursor protein: beyond Alzheimer's disease (pages 756–769)

      Edgar Dawkins and David H. Small

      Version of Record online: 7 MAR 2014 | DOI: 10.1111/jnc.12675

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      This article reviews studies on the structure, expression and post-translational processing of β-amyloid precursor protein (APP), as well as studies on the effects of APP in vitro and in vivo. We conclude that the published data provide strong evidence that APP has a trophic function. APP is likely to be involved in neural stem cell development, neuronal survival, neurite outgrowth and neurorepair. However, the mechanisms by which APP exerts its actions remain to be elucidated. The available evidence suggests that APP interacts both intracellularly and extracellularly to regulate various signal transduction mechanisms.

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      Impaired one carbon metabolism and DNA methylation in alcohol toxicity (pages 770–780)

      Inna I. Kruman and Anna-Kate Fowler

      Version of Record online: 7 MAR 2014 | DOI: 10.1111/jnc.12677

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      In this review, we summarize the role of one-carbon metabolism (OCM) aberrations in chronic alcohol-induced toxicity. OCM is a major donor of methyl groups for methylation reactions, particularly DNA methylation critical for epigenetic regulation of gene expression. Alcohol interference with OCM and consequent reduced availability of methyl groups, improper DNA methylation, and aberrant gene expression can play a causative role in alcohol toxicity.

  6. HIGHLIGHTED ARTICLE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
    1. ORIGINAL ARTICLES

      Signal Transduction & Synaptic Transmission
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      Botulinum protease-cleaved SNARE fragments induce cytotoxicity in neuroblastoma cells (pages 781–791)

      Jason Arsenault, Sabine A. G. Cuijpers, Enrico Ferrari, Dhevahi Niranjan, Aleksander Rust, Charlotte Leese, John A. O'Brien, Thomas Binz and Bazbek Davletov

      Version of Record online: 23 JAN 2014 | DOI: 10.1111/jnc.12645

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      Ternary complex formation by synaptobrevin (green) and syntaxin/synaptosomal-associated protein of 25 kDa (red) is necessary for vesicle fusion, membrane trafficking, and cell homeostasis. Botulinum proteases cleave the three SNAREs proteins as indicated, resulting in a loss of cell viability. Lipofection reagents were used to deliver botulinum proteases or short SNARE peptides into neuroblastoma cells, revealing cytotoxic effects of SNARE fragments.

      Read the Editorial Highlight for this article on page 753.

  7. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. HIGHLIGHTED ARTICLE
    8. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Choline-mediated modulation of hippocampal sharp wave–ripple complexes in vitro (pages 792–805)

      Viktoria Fischer, Martin Both, Andreas Draguhn and Alexei V. Egorov

      Version of Record online: 19 MAR 2014 | DOI: 10.1111/jnc.12693

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      In this study we asked whether choline, the precursor and degradation product of acetylcholine, directly affects hippocampal network activity. Using mouse hippocampal slices we found that choline efficiently suppresses spontaneously occurring sharp wave–ripple complexes (SPW-R). In addition, choline reduces synaptic transmission between hippocampal subfields. These effects are mediated by direct activation of muscarinic as well as nicotinic cholinergic pathways. Together, choline turns out to be a potent regulator of patterned activity within hippocampal networks.

    2. Bioenergetics & Metabolism

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      In vivo brain macromolecule signals in healthy and glioblastoma mouse models: 1H magnetic resonance spectroscopy, post-processing and metabolite quantification at 14.1 T (pages 806–815)

      Mélanie Craveiro, Virginie Clément-Schatlo, Denis Marino, Rolf Gruetter and Cristina Cudalbu

      Version of Record online: 26 FEB 2014 | DOI: 10.1111/jnc.12673

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      In 1H magnetic resonance spectroscopy, the precise knowledge of the macromolecule signals is essential. After introducing a novel method for a flexible and robust post-processing of measured macromolecule signals, the absence of significant differences in metabolite quantification as a result of regional macromolecule variability was demonstrated in the mouse brain while several alterations of the macromolecule spectrum were observed in a mouse model of human glioma.

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      Inhibition of Rho-kinase protects cerebral barrier from ischaemia-evoked injury through modulations of endothelial cell oxidative stress and tight junctions (pages 816–826)

      Claire L. Gibson, Kirtiman Srivastava, Nikola Sprigg, Philip M. W. Bath and Ulvi Bayraktutan

      Version of Record online: 18 MAR 2014 | DOI: 10.1111/jnc.12681

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      Inhibition of Rho-kinase (ROCK) activity in a mouse model of human ischaemic stroke significantly improved functional outcome while reducing cerebral lesion and oedema volumes compared to vehicle-treated counterparts. Studies conducted with brain microvascular endothelial cells exposed to OGD ± R in the presence of Y-27632 revealed restoration of intercellular junctions and suppression of prooxidant NADPH oxidase activity as important factors in ROCK inhibition-mediated BBB protection.

    4. Neuroinflammation & Neuroimmunology

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      Hydrogen sulfide protects blood–brain barrier integrity following cerebral ischemia (pages 827–838)

      Yali Wang, Jia Jia, Guizhen Ao, Lifang Hu, Hui Liu, Yunqi Xiao, Huaping Du, Nabil J. Alkayed, Chun-Feng Liu and Jian Cheng

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12695

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      To determine H2S effects on blood–brain barrier (BBB) disruption following stroke, we used two structurally unrelated H2S donors ADT and NaHS. Both ADT and NaHS remarkably protected BBB integrity following experimental stroke. The slow-releasing donor ADT also reduced post-ischemic inflammation-induced expression and activity of MMP9 and NOX4 in the ischemic brain possibly by inhibiting NF-κB activation.

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      2,3,7,8-Tetrachlorodibenzo-p-dioxin promotes astrocyte activation and the secretion of tumor necrosis factor-α via PKC/SSeCKS-dependent mechanisms (pages 839–849)

      Yang Zhang, Xiaoke Nie, Tao Tao, Wenbo Qian, Shengyang Jiang, Junkang Jiang, Aihong Li, Aisong Guo, Guangfei Xu and Qiyun Wu

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12696

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      2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) elicits neurotoxic effects. Here, we show TCDD induces pro-inflammatory responses in astrocytes. TCDD initiates an increase of [Ca2+]i, followed by the activation of PKC, which then induces the activation of Src-suppressed C-kinase substrate (SSeCKS). SSeCKS promotes NF-κB activation and the secretion of TNF-α and nitric oxide in astrocytes.

    6. Neuronal Plasticity & Behavior

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      Targeted gene mutation of E2F1 evokes age-dependent synaptic disruption and behavioral deficits (pages 850–863)

      Jenhao H. Ting, David R. Marks, Stephanie S. Schleidt, Joanna N. Wu, Jacob W. Zyskind, Kathryn A. Lindl, Julie A. Blendy, R. Christopher Pierce and Kelly L. Jordan-Sciutto

      Version of Record online: 12 FEB 2014 | DOI: 10.1111/jnc.12655

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      E2F1 is a transcription factor regulating cell cycle progression and apoptosis. Although E2F1 dysregulation under toxic conditions can lead to neuronal death, little is known about its physiologic activity in the healthy brain. Here, we report significant age-dependent olfactory and memory deficits in mice with dysfunctional E2F1. Coincident with these behavioral changes, we also found age-matched synaptic disruption and persisting reduction in adult neurogenesis. Our study demonstrates that E2F1 contributes to physiologic brain structure and function.

      Cover Image for this issue: doi: 10.1111/jnc.12561.

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      A new semisynthetic derivative of sauroine induces LTP in hippocampal slices and improves learning performance in the Morris Water Maze (pages 864–876)

      Mariana Vallejo, Sebastián Loyola, Darwin Contreras, Gonzalo Ugarte, Diego Cifuente, Gabriela Ortega, José L. Cabrera, Marc Zeise, Carlos Tonn, Mario Carreño, Ricardo Delgado, Bernardo Morales and Mariel Agnese

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12685

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      A semisynthetic derivative of sauroine, diacetyl sauroine (DAS), induces chemical long-term potentiation in rat hippocampal slices increasing the NMDA receptor-dependent current. 2 mg/kg prior to each session in a Morris Water Maze (MWM) improves behavior performance. In slices prepared from the tested rats the electrical stimulation-dependent long-term potentiation (LTP) was greatly enhanced. Therefore, DAS may have potency as a nootropic drug against the memory decline.

    8. Molecular Basis of Disease

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      Serum miR-206 and other muscle-specific microRNAs as non-invasive biomarkers for Duchenne muscular dystrophy (pages 877–883)

      Jun Hu, Min Kong, Yuanzhen Ye, Siqi Hong, Li Cheng and Li Jiang

      Version of Record online: 12 FEB 2014 | DOI: 10.1111/jnc.12662

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      There has been a long-standing need for reliable, non-invasive biomarkers for Duchenne muscular dystrophy (DMD). We found that the levels of muscle-specific microRNAs, especially miR-206, in the serum of DMD were 2- to 4-fold higher than in the controls. High levels corresponded to low muscle strength, muscle function, and quality of life (QoL). These miRNAs were able to discriminate DMD from controls by receiver operating characteristic (ROC) curves analyses. Thus, miR-206 and other muscle-specific miRNAs are useful as non-invasive biomarkers for DMD.

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      Inhibition of glucosylceramide synthase stimulates autophagy flux in neurons (pages 884–894)

      Wei Shen, Anastasia G. Henry, Katrina L. Paumier, Li Li, Kewa Mou, John Dunlop, Zdenek Berger and Warren D. Hirst

      Version of Record online: 3 MAR 2014 | DOI: 10.1111/jnc.12672

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      Inhibition of GlcCer synthase enhances autophagy by inhibiting AKT-mTOR signaling, and increases the number and size of lysosomal/late endosomal structures. Furthermore, inhibition of GlcCer synthase decreased levels of mutant α-synuclein in neurons, which may represent a potential therapeutic target for Parkinson's disease.

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