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Journal of Neurochemistry

Cover image for Vol. 130 Issue 1

July 2014

Volume 130, Issue 1

Pages i–ix, 1–160

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. PREFACE
    6. REVIEW
    7. ORIGINAL ARTICLES
    8. CORRIGENDUM
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      Issue Cover (July 2014)

      Version of Record online: 20 JUN 2014 | DOI: 10.1111/jnc.12568

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      Front cover: Atomic force microscopy images collected to confirm the pre-aggregation of Aβ[1-42] into fibril structures (cover image) or oligomer structures (not shown). Aβ[1-42] is colored pink against the blue background. Scale bar is 500 nm. J. Neurochem. 2014, vol. 130 (1), pp. 136–144.

      Read the full article on doi: 10.1111/jnc.12678

  2. Issue Information

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

      Version of Record online: 20 JUN 2014 | DOI: 10.1111/jnc.12569

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. PREFACE
    6. REVIEW
    7. ORIGINAL ARTICLES
    8. CORRIGENDUM
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      In this Issue (pages iii–ix)

      Version of Record online: 20 JUN 2014 | DOI: 10.1111/jnc.12570

  4. PREFACE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. PREFACE
    6. REVIEW
    7. ORIGINAL ARTICLES
    8. CORRIGENDUM
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      Neuroinflammation: good, bad, or indifferent? (pages 1–3)

      Tammy Kielian

      Version of Record online: 24 MAY 2014 | DOI: 10.1111/jnc.12755

      This is the Preface for the Virtual Issue: “Neuroinflammation in Nervous System Disorders: Diversity in Insults and Outcomes”: http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159/homepage/virtual_issues.htm#neuroinflammation

  5. REVIEW

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. PREFACE
    6. REVIEW
    7. ORIGINAL ARTICLES
    8. CORRIGENDUM
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      Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects (pages 4–28)

      Robert Vassar, Peer-Hendrik Kuhn, Christian Haass, Matthew E. Kennedy, Lawrence Rajendran, Philip C. Wong and Stefan F. Lichtenthaler

      Version of Record online: 19 APR 2014 | DOI: 10.1111/jnc.12715

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      The protease BACE1 is a major drug target in Alzheimer disease. Together with its homolog BACE2, both proteases have an increasing number of functions within and outside of the nervous system. This review highlights recent progress in understanding cell biology, substrates, and functions of BACE proteases and discusses the therapeutic options and potential mechanism-based liabilities, in particular for BACE inhibitors in Alzheimer disease.

  6. ORIGINAL ARTICLES

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

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      Contribution of cysteine aminotransferase and mercaptopyruvate sulfurtransferase to hydrogen sulfide production in peripheral neurons (pages 29–40)

      Ryo Miyamoto, Ken-ichi Otsuguro, Soichiro Yamaguchi and Shigeo Ito

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12698

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      In the peripheral nervous system, hydrogen sulfide (H2S) has been implicated in neurogenic pain or hyperalgesia. This study provides evidence that H2S is synthesized in peripheral neurons through two mitochondrial enzymes, cysteine aminotransferase (CAT) and mercaptopyruvate sulfurtransferase (MPST). We propose that mitochondrial metabolism plays key roles in the physiology and pathophysiology of the peripheral nervous system via regulation of neuronal H2S production.

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      Targeted inhibition of KCa3.1 attenuates TGF-β-induced reactive astrogliosis through the Smad2/3 signaling pathway (pages 41–49)

      Zhihua Yu, Panpan Yu, Hongzhuan Chen and Herbert M. Geller

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12710

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      Reactive astrogliosis is characterized by the expression of glial fibrillary acidic protein and chondroitin sulfate proteoglycans. We demonstrate that either pharmacological blockade or knockout of KCa3.1 channels reduces reactive gliosis in cultured astrocytes caused by TGF-β, and also reduces TGF-β-induced phosphorylation of Smad2/3.

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      Mechanical stimulation evokes rapid increases in extracellular adenosine concentration in the prefrontal cortex (pages 50–60)

      Ashley E. Ross, Michael D. Nguyen, Eve Privman and B. Jill Venton

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12711

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      We have discovered immediate changes in adenosine concentration in the prefrontal cortex following mechanical stimulation. The adenosine increase lasts only about 20 s. Mechanically stimulated adenosine was activity dependent and mostly because of extracellular ATP metabolism. This rapid, transient increase in adenosine may help protect tissue and would occur during implantation of any electrode, such as during deep brain stimulation.

    4. Bioenergetics & Metabolism

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      Guanosine protects C6 astroglial cells against azide-induced oxidative damage: a putative role of heme oxygenase 1 (pages 61–74)

      André Quincozes-Santos, Larissa Daniele Bobermin, Débora Guerini Souza, Bruna Bellaver, Carlos-Alberto Gonçalves and Diogo Onofre Souza

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12694

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      Guanosine protects against azide-induced oxidative damage in C6 astroglial cells. Azide-induced mitochondrial dysfunction (1); increased reactive oxygen species/reactive nitrogen species levels (2); decreased glutamate uptake (3), GS activity (4), GSH levels (5), and SOD (6) and CAT (7) activities; increased glutathione peroxidase (GPx) (8) and NADPH oxidase (9) activities and cellular superoxide levels (10); increased NF-κB activation (11), TNF-α and IL-1β levels (12); and induced iNOS expression (13). Guanosine prevented these effects through the HO1 signaling pathway, thus our findings support the antioxidant effects of guanosine.

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      Stable over-expression of the 2-oxoglutarate carrier enhances neuronal cell resistance to oxidative stress via Bcl-2-dependent mitochondrial GSH transport (pages 75–86)

      Heather M. Wilkins, Samantha Brock, Josie J. Gray and Daniel A. Linseman

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12709

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      Stable over-expression of the 2-oxoglutarate carrier (OGC) in a motor neuronal cell line induced a specific increase in mitochondrial GSH and markedly enhanced resistance to oxidative stress. Over-expression of OGC also induced Bcl-2 expression which was owing to the specific increase in mitochondrial GSH. Intriguingly, enhanced expression of Bcl-2 was required to sustain OGC-dependent GSH transport into the mitochondria. Thus, OGC and Bcl-2 work in a concerted manner to maintain the mitochondrial GSH pool which is crucial for neuronal survival.

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      Proton-dependent zinc release from intracellular ligands (pages 87–96)

      Lech Kiedrowski

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12712

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      This study aimed at identifying intracellular stores which release Zn2+ when pHi drops from 6.6 to 6.1. It was found that these stores are not mitochondria or acidic organelles, but rather intracellular Zn2+ ligands. When the pH was decreasing from 6.6 to 6.1, only zinc–cysteine complexes showed a rapid acceleration in the rate of Zn2+ release. Therefore, the stores responsible for an acid-induced intracellular Zn2+ release in neurons may be the cytosolic zinc–cysteine complexes.

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      The enzyme lecithin-cholesterol acyltransferase esterifies cerebrosterol and limits the toxic effect of this oxysterol on SH-SY5Y cells (pages 97–108)

      Valeria La Marca, Maria Stefania Spagnuolo, Luisa Cigliano, Daniela Marasco and Paolo Abrescia

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12713

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      24-hydroxycholesterol (24(S)OH-C) is neurotoxic. The enzyme lecithin-cholesterol acyltransferase (LCAT) synthesizes monoesters of 24(S)OH-C in reaction mixtures with proteoliposomes containing phospholipids and apolipoprotein A-I or apolipoprotein E. The esters, also produced by incubation of cerebrospinal fluid only with tritiated 24(S)OH-C, are embedded into lipoproteins that do not enter neurons in culture. The enzyme activity limits the toxicity of 24-hydroxycholesterol in neuron culture.

    8. Neuronal Plasticity & Behavior

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      Dopamine denervation of the prefrontal cortex increases expression of the astrocytic glutamate transporter GLT-1 (pages 109–114)

      Peter J. Vollbrecht, Linda D. Simmler, Randy D. Blakely and Ariel Y. Deutch

      Version of Record online: 18 MAR 2014 | DOI: 10.1111/jnc.12697

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      The glutamate transporter GLT-1 is expressed by astrocytes, which also express dopamine receptors. Regulation of prefrontal cortical (PFC) GLT-1 potentially offers a novel treatment approach to the cognitive deficits of schizophrenia. Partial PFC dopamine deafferentation increased membrane expression of GLT-1 protein and glutamate uptake, but did not alter levels of the other two neocortical glutamate transporters, GLAST and EAAC1.

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      Down-regulation of serum gonadotropins but not estrogen replacement improves cognition in aged-ovariectomized 3xTg AD female mice (pages 115–125)

      Russell Palm, Jaewon Chang, Jeffrey Blair, Yoelvis Garcia-Mesa, Hyoung-gon Lee, Rudy J. Castellani, Mark A. Smith, Xiongwei Zhu and Gemma Casadesus

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12706

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      In the aged triple transgenic Alzheimer's disease (AD) mouse model (3xAD-Tg), estrogen replacement after ovariectomy does not improve cognitive function, increases phosphorylated Tau levels and decreases inhibition of GSK3 beta. Luprolide acetate rescues ovariectomy-dependent cognitive function, increases signaling events associated with synaptic plasticity including GSK3 beta inhibition, but does not alter AD pathology. In the human AD female brain, luteinizing hormone (LH) mRNA levels are reduced. In the 3XAD-tg model, brain LH protein levels are reduced by ovariectomy and normalized by leuprolide acetate treatment. These treatment-dependent normalization of LH positively correlates with markers of neuroplasticity and cognitive improvement.

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      Relationships between serotonergic and cannabinoid system in depressive-like behavior: a PET study with [11C]-DASB (pages 126–135)

      Aurelijus Burokas, Elena Martín-García, Javier Gutiérrez-Cuesta, Santiago Rojas, José Raúl Herance, Juan Domingo Gispert, Miquel-Ángel Serra and Rafael Maldonado

      Version of Record online: 30 APR 2014 | DOI: 10.1111/jnc.12716

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      Chronic restraint stress induces depressive-like behavior and reduced 5-HTT levels in WT mice similar to those revealed in non-stressed CB1-KO mice. Reduced 5-HTT in both genotypes increases synaptic 5-HT concentration. The 5-HT release is modulated through CB1 receptors and the absence of inhibitory CB1 receptor causes decreased inhibition of 5-HT release resulting in high synaptic 5-HT concentration that are not further enhanced by stress.

    11. Molecular Basis of Disease

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      Amyloid-β concentration and structure influences the transport and immunomodulatory effects of IVIG (pages 136–144)

      Diane M. Wuest and Kelvin H. Lee

      Version of Record online: 6 MAR 2014 | DOI: 10.1111/jnc.12678

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      The mechanisms of action and transport across the blood–brain barrier (BBB) for an Alzheimer's disease therapeutic, intravenous immunoglobulin (IVIG), remain unknown. We investigated the transport of IVIG across endothelial cell BBB monolayers pre-incubated with amyloid-β peptides. We found that the concentration and structure of amyloid-β plays an important role in the effect of IVIG on BBB tightening and cytokine neutralization. (Note: Figure not drawn to scale.)

      Cover Image for this issue: doi: 10.1111/jnc.12568.

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      Alterations in STriatal-Enriched protein tyrosine Phosphatase expression, activation, and downstream signaling in early and late stages of the YAC128 Huntington's disease mouse model (pages 145–159)

      Clare M. Gladding, Jing Fan, Lily Y. J. Zhang, Liang Wang, Jian Xu, Edward H. Y. Li, Paul J. Lombroso and Lynn A. Raymond

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12700

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      The YAC128 Huntington's disease mouse model shows early, enhanced susceptibility to NMDA receptor-mediated striatal apoptosis, progressing to late-stage excitotoxicity resistance. This study shows that elevated NMDA receptor–PSD-95 interactions as well as decreased extrasynaptic STriatal-Enriched protein tyrosine Phosphatase 61 (STEP61) activation may contribute to early enhanced apoptotic signaling. In late-stage YAC128 mice, reduced STEP61 levels and activity correlate with elevated MAPK signaling, consistent with excitotoxicity resistance. Solid and dotted arrows indicate conclusions drawn from the current study and other literature, respectively.

  7. CORRIGENDUM

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. PREFACE
    6. REVIEW
    7. ORIGINAL ARTICLES
    8. CORRIGENDUM
    1. You have free access to this content
      Corrigendum (page 160)

      Version of Record online: 22 MAY 2014 | DOI: 10.1111/jnc.12749

      This article corrects:

      Involvement of α2-antiplasmin in dendritic growth of hippocampal neurons

      Vol. 126, Issue 1, 58–69, Version of Record online: 22 MAY 2013

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