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Journal of Neurochemistry

Cover image for Vol. 127 Issue 4

November 2013

Volume 127, Issue 4

Pages i–xi, 434–574

  1. IN THIS ISSUE

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
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      In this Issue (pages i–xi)

      Version of Record online: 4 NOV 2013 | DOI: 10.1111/jnc.12485

  2. PREFACE

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
    1. You have free access to this content
  3. EDITORIAL HIGHLIGHT

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
    1. You have free access to this content
  4. REVIEW ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
    1. You have free access to this content
      Harnessing the power of yeast to unravel the molecular basis of neurodegeneration (pages 438–452)

      Sandra Tenreiro, Matthias C. Munder, Simon Alberti and Tiago F. Outeiro

      Version of Record online: 8 MAY 2013 | DOI: 10.1111/jnc.12271

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      Drosophila as a screening tool to study human neurodegenerative diseases (pages 453–460)

      Sarah Lenz, Peter Karsten, Jörg B. Schulz and Aaron Voigt

      Version of Record online: 20 OCT 2013 | DOI: 10.1111/jnc.12446

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  5. HIGHLIGHTED ARTICLE

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
    1. ORIGINAL ARTICLE

      Molecular Basis of Disease
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      Loss of Bace2 in zebrafish affects melanocyte migration and is distinct from Bace1 knock out phenotypes (pages 471–481)

      Frauke van Bebber, Alexander Hruscha, Michael Willem, Bettina Schmid and Christian Haass

      Version of Record online: 11 MAR 2013 | DOI: 10.1111/jnc.12198

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      Inhibition of BACE1 protease activity has therapeutic importance for Alzheimer's disease. Analysis of BACE1 and BACE2 knock-out zebrafish revealed that they exhibit distinct phenotypes. bace1 mutants display hypomyelination in the PNS and supernumerary neuromasts while in bace2 mutants the shape and migration of melanocytes is affected. These phenotypes are not further enhanced in the viable double mutants. Our data suggest that blocking BACE1 activity is a safe therapeutic approach.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12200.

  6. SHORT COMMUNICATION

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
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      Vesicular GABA transporter (VGAT) transports β-alanine (pages 482–486)

      Narinobu Juge, Hiroshi Omote and Yoshinori Moriyama

      Version of Record online: 26 AUG 2013 | DOI: 10.1111/jnc.12393

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      Vesicular GABA transporter (VGAT) is expressed in GABAergic and glycinergic neurons, and is responsible for vesicular storage and subsequent exocytosis of these inhibitory amino acids. In the present study, we showed that proteoliposomes containing purified VGAT transport β-alanine using Δψ as a driving force. VGAT also facilitates Cl uptake. Our findings indicated that VGAT functions as a vesicular β-alanine transporter.

  7. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. PREFACE
    4. EDITORIAL HIGHLIGHT
    5. REVIEW ARTICLES
    6. HIGHLIGHTED ARTICLE
    7. SHORT COMMUNICATION
    8. ORIGINAL ARTICLES
    1. Gene Regulation & Genetics

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      Estrogen receptor-β regulates human tryptophan hydroxylase-2 through an estrogen response element in the 5′ untranslated region (pages 487–495)

      Ryoko Hiroi and Robert J. Handa

      Version of Record online: 18 SEP 2013 | DOI: 10.1111/jnc.12401

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      We illustrate a direct regulation of the TPH2 transcription by estradiol and ERβ via a newly identified ERE half-site within the TPH2 promoter: (i) Estradiol- or an ERβ agonist-induced TPH2 transcription was blocked by an ER antagonist, while (ii) membrane impermeable form of estradiol did not induce transcription. (iii) Deletion or mutation of the ERE half-site abolished ligand-induced TPH2 transcription.

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      Neuron-specific specificity protein 4 bigenomically regulates the transcription of all mitochondria- and nucleus-encoded cytochrome c oxidase subunit genes in neurons (pages 496–508)

      Kaid Johar, Anusha Priya, Shilpa Dhar, Qiuli Liu and Margaret T. T. Wong-Riley

      Version of Record online: 30 SEP 2013 | DOI: 10.1111/jnc.12433

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      The present study discovered that among the specificity family of transcription factors, it is the less known neuron-specific Sp4 that regulates the expression of all 13 subunits of mitochondrial cytochrome c oxidase (COX) enzyme in primary neurons. Sp4 also regulates the three mitochondrial transcription factors (TFAM, TFB1M, and TFB2M) and a COX assembly protein SURF-1 in primary neurons.

    3. Signal Transduction & Synaptic Transmission

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      Urban air pollutants reduce synaptic function of CA1 neurons via an NMDA/NȮ pathway in vitro (pages 509–519)

      David A. Davis, Garnik Akopian, John P. Walsh, Constantinos Sioutas, Todd E. Morgan and Caleb E. Finch

      Version of Record online: 26 AUG 2013 | DOI: 10.1111/jnc.12395

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      We present three new findings of rapid hippocampal slice responses to nPM (nano-sized particulate matter from urban traffic): increased NȮ production within 15 min; nitrosylation of glutamatergic NMDA receptors; and, reduced excitatory postsynaptic currents in CA1 neurons. AP5 (NMDA receptor antagonist) blocked nPM-mediated NȮ and receptor nitrosylation. Ca2+ influx is a likely mechanism.

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      Effects of essential amino acid deficiency: down-regulation of KCC2 and the GABAA receptor; disinhibition in the anterior piriform cortex (pages 520–530)

      James W. Sharp, Catherine M. Ross-Inta, Irène Baccelli, John A. Payne, John B. Rudell and Dorothy W. Gietzen

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/jnc.12403

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      The circuitry of the anterior piriform cortex (APC) is finely balanced between excitatory (glutamate, +) and inhibitory (GABA, −) transmission. GABAA receptors use Cl, requiring the neural potassium chloride co-transporter (KCC2). Both are rapidly turning-over proteins, dependent on protein synthesis for repletion. In IAA (indispensable amino acid) deficiency, within 20 min, blockade of protein synthesis prevents restoration of these inhibitors; they are diminished; disinhibition ensues. GCN2 = general control non-derepressing kinase 2, eIF2α = α-subunit of the eukaryotic initiation factor 2.

    5. Neuronal Plasticity & Behavior

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      Growth hormone releasing hormone (GHRH) signaling modulates intermittent hypoxia-induced oxidative stress and cognitive deficits in mouse (pages 531–540)

      Deepti Nair, Vijay Ramesh, Richard C. Li, Andrew V. Schally and David Gozal

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12360

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      Sleep apnea, characterized by chronic intermittent hypoxia (IH), is associated with substantial cognitive and behavioral deficits. Here, we show that administration of a GHRH agonist (JI-34) reduces oxidative stress, increases both HIF-1α nuclear binding and downstream expression of IGF1 and erythropoietin (EPO) in hippocampus and cortex, and markedly attenuates water maze performance deficits in mice exposed to intermittent hypoxia during sleep.

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      Intravenous nicotine injection induces rapid, experience-dependent sensitization of glutamate release in the ventral tegmental area and nucleus accumbens (pages 541–551)

      Magalie Lenoir and Eugene A. Kiyatkin

      Version of Record online: 20 OCT 2013 | DOI: 10.1111/jnc.12450

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      By using high-speed amperometry with glutamate (GLU) biosensors, we show that i.v. nicotine at a low, behaviorally relevant dose induces rapid GLU release in the NAcc and VTA that is enhanced following repeated drug injections. This is the first study reporting second-scale fluctuations in extracellular GLU levels induced by nicotine in two critical structures of the motivation-reinforcement circuit and rapid sensitization of GLU responses coupled with locomotor sensitization.

    7. Molecular Basis of Disease

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      Specific subcellular changes in oxidative stress in prefrontal cortex from patients with bipolar disorder (pages 552–561)

      Ana C. Andreazza, Jun-Feng Wang, Faraz Salmasi, Li Shao and Lionel T. Young

      Version of Record online: 11 JUN 2013 | DOI: 10.1111/jnc.12316

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      Oxidative stress has been shown to be higher in the brain of patients with bipolar disorder (BD). Here, we demonstrated increased levels of protein oxidation in synaptosomes from postmortem prefrontal cortex from patients from BD group, while 3-nitrotyrosine was increased in mitochondria from BD and schizophrenia (SCZ) groups. Moreover, lipid peroxidation was found increased in the BD when compared with controls; suggesting that in BD mitochondrial proteins are more susceptible to potentially reversible nitrosative damage while more longstanding oxidative damage occurs to synaptic proteins.

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      Neuroprotective effects of donepezil against Aβ42-induced neuronal toxicity are mediated through not only enhancing PP2A activity but also regulating GSK-3β and nAChRs activity (pages 562–574)

      Min-Young Noh, Seong H. Koh, Sung-Min Kim, Tangui Maurice, Sae-Kwang Ku and Seung H. Kim

      Version of Record online: 17 JUN 2013 | DOI: 10.1111/jnc.12319

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      We investigated neuroprotective mechanisms of donepezil against Aβ42 toxicity: Donepezil increased neuronal viability with reduced p-tau by enhancing PP2A activity. Despite of blocked PP2A activity, donepezil showed additional recovering effect on neuronal viability, which findings led us to assume that additional mechanisms of donepezil including its inhibitory effect on GSK-3β activity and activating role of nicotinic AChRs might be involved.

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