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Journal of Neurochemistry

Cover image for Vol. 126 Issue 2

July 2013

Volume 126, Issue 2

Pages 145–300

  1. EDITORIAL

    1. Top of page
    2. EDITORIAL
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
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  2. REVIEW ARTICLES

    1. Top of page
    2. EDITORIAL
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    1. You have free access to this content
      Vesicle dynamics: how synaptic proteins regulate different modes of neurotransmission (pages 146–154)

      ChiHye Chung and Jesica Raingo

      Article first published online: 23 APR 2013 | DOI: 10.1111/jnc.12245

      Corrected by:

      Corrigendum: Corrigendum

      Vol. 128, Issue 2, 340, Article first published online: 10 DEC 2013

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      Actin filaments and microtubules in dendritic spines (pages 155–164)

      Tomoaki Shirao and Christian González-Billault

      Article first published online: 11 JUN 2013 | DOI: 10.1111/jnc.12313

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      Developmental vulnerability of synapses and circuits associated with neuropsychiatric disorders (pages 165–182)

      Peter Penzes, Andres Buonanno, Maria Passafaro, Carlo Sala and Robert A. Sweet

      Article first published online: 22 MAY 2013 | DOI: 10.1111/jnc.12261

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      From synaptic spines to nuclear signaling: nuclear and synaptic actions of the amyloid precursor protein (pages 183–190)

      Jean-Noël Octave, Nathalie Pierrot, Susana Ferao Santos, Natalia N. Nalivaeva and Anthony J. Turner

      Article first published online: 3 APR 2013 | DOI: 10.1111/jnc.12239

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      So far, no new therapeutic agents for Alzheimer's disease (AD) have reached the clinics based on reducing amyloid β-peptide (Aβ) levels through the use of secretase inhibitors or immunotherapy. Here, we highlight emerging areas of amyloid precursor protein (APP) function that may provide new insights into synaptic development, cognition, and gene regulation. Endogenous APP in primary cortical neurons has a key role in maintaining neuronal calcium homeostasis essential for synaptic transmission. Disruption of this homeostatic mechanism predisposes to aging and AD. The intracellular domain of APP (AICD) is also a key epigenetic regulator of various genes, including APP itself, the amyloid-degrading enzyme neprilysin (NEP), and aquaporin-1.

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      Deregulation of excitatory neurotransmission underlying synapse failure in Alzheimer's disease (pages 191–202)

      Andrea C. Paula-Lima, Jordano Brito-Moreira and Sergio T. Ferreira

      Article first published online: 28 MAY 2013 | DOI: 10.1111/jnc.12304

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      STED microscopy of living cells – new frontiers in membrane and neurobiology (pages 203–212)

      Christian Eggeling, Katrin I. Willig and Francisco J. Barrantes

      Article first published online: 23 APR 2013 | DOI: 10.1111/jnc.12243

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  3. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Stapling of the botulinum type A protease to growth factors and neuropeptides allows selective targeting of neuroendocrine cells (pages 223–233)

      Jason Arsenault, Enrico Ferrari, Dhevahi Niranjan, Sabine A. G. Cuijpers, Chunjing Gu, Yvonne Vallis, John O'Brien and Bazbek Davletov

      Article first published online: 20 MAY 2013 | DOI: 10.1111/jnc.12284

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      Botulinum neurotoxin is an excellent tool for causing prolonged blockade of secretion offering the possibility of targeted modulation of neuroendocrine functions. We now show the potential of our new protein stapling technique for combinatorial and on-demand assembly of the botulinum enzyme with growth factors and neuropeptides to retarget the botulinum activity into desired cell populations for biomedical applications.

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      Cleavage of GSK-3β by calpain counteracts the inhibitory effect of Ser9 phosphorylation on GSK-3β activity induced by H2O2 (pages 234–242)

      Ye Feng, Yiyuan Xia, Guang Yu, Xiji Shu, Haoliang Ge, Kuan Zeng, Jianzhi Wang and Xiaochuan Wang

      Article first published online: 30 MAY 2013 | DOI: 10.1111/jnc.12285

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      GSK-3β dysfunction is critical in the pathogenesis of psychiatric, metabolic, neurodegenerative diseases, in which oxidative stress exists concurrently. Under H2O2 condition, Akt (also known as Protein Kinase B, PKB) activation increases phospho-Ser9 of glycogen synthase kinase (GSK)-3β, an inactivated form of GSK-3β. Simultaneously, calpain activation leads to GSK-3β truncation, which in turn overrides the inhibitory effect of Ser9 phosphorylation, up-regulates GSK-3β activity.

    3. Neuroinflammation & Neuroimmunology

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      Retinal cell type-specific prevention of ischemia-induced damages by LPS-TLR4 signaling through microglia (pages 243–260)

      Sebok K. Halder, Hayato Matsunaga, Ken J. Ishii, Shizuo Akira, Kensuke Miyake and Hiroshi Ueda

      Article first published online: 13 MAY 2013 | DOI: 10.1111/jnc.12262

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      We proposed the following mechanism for LPS preconditioning-induced retinal prevention against ischemia: LPS preconditioning-induced retinal prevention against ischemic damages is mediated by toll-like receptor (TLR4) signaling through microglia. This TLR4 priming by LPS preconditioning dominantly activates TRIF-IRF3 (TIR-domain-containing adapter-inducing interferon-β/interferon regulatory factor 3) pathway and suppresses MyD88 - NF-κB pathway. Thus, detailed study of these findings may provide novel idea for discovery of new drugs against ischemic disorders.

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      Ethanol induces TLR4/TLR2 association, triggering an inflammatory response in microglial cells (pages 261–273)

      Sara Fernandez-Lizarbe, Jorge Montesinos and Consuelo Guerri

      Article first published online: 8 MAY 2013 | DOI: 10.1111/jnc.12276

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      We have shown that ethanol promotes TLR4 activation through its interactions with the lipid rafts microdomains. Here, we report that ethanol triggers TLR4/TLR2 recruitment into microglia lipid rafts/caveolae, promoting TLR4 and TLR2 interactions and signaling and leading to the production of proinflammatory cytokines, which cause ROS generation and neuronal apoptosis. These findings might provide a mechanism for alcohol-triggered neuroinflammation and brain damage.

    5. Molecular Basis of Disease

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      Calmodulin Kinase IV–dependent CREB activation is required for neuroprotection via NMDA receptor-PSD95 disruption (pages 274–287)

      Karen F. S. Bell, Russell J. Bent, Saira Meese-Tamuri, Alicia Ali, Joan P. Forder and Michelle M. Aarts

      Article first published online: 3 MAR 2013 | DOI: 10.1111/jnc.12176

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      We propose that uncoupling NMDA receptors from PSD95 provides neuroprotection from stroke by enhancing Ca2+/Calmodulin-dependent neurotrophic signalling. Blocking NMDAR-PSD95 interactions allows enhanced activation of nuclear CaM-kinase IV and prolonged phosphorylation of the CREB transcription factor, resulting in enhanced neurotrophic transcription. These findings demonstrate the importance of maintaining neurotrophic, Ca2 + -dependent signalling during neuronal injury and provide novel targets for neuroprotection in stroke.

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      TDP-43 associates with stalled ribosomes and contributes to cell survival during cellular stress (pages 288–300)

      Shinji Higashi, Tomohiro Kabuta, Yoshitaka Nagai, Yukihiro Tsuchiya, Haruhiko Akiyama and Keiji Wada

      Article first published online: 1 MAR 2013 | DOI: 10.1111/jnc.12194

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      TDP-43 is an important contributor to ALS and FTLD. In this study, we revealed that TDP-43 associates with stalled ribosomes and that its silencing disturbs mRNA stability and cell survival during cellular stress. Our findings suggest that TDP-43 is a stress-response protein that functions in translational control mechanisms and determines cell survival.

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