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Journal of Neurochemistry

Cover image for Vol. 128 Issue 6

March 2014

Volume 128, Issue 6

Pages i–x, 787–977

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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      Issue Cover (March 2014)

      Version of Record online: 7 MAR 2014 | DOI: 10.1111/jnc.12545

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      Front cover: Immunocytochemistry reveals the subcellular localization of the synaptically-driven S-Q phosphoproteome (red: high, blue: low) in an individual primary cortical neuron. J. Neurochem. 2014, vol. 128 (6), pp. 841–851.

      Read the full article on doi: 10.1111/jnc.12487

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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      Issue Information (pages i–ii)

      Version of Record online: 7 MAR 2014 | DOI: 10.1111/jnc.12546

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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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. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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      Cytosolic PINK1 escapes from mitochondria to promote dendritic outgrowth (pages 787–789)

      Kim Tieu and Xu-Gang Xia

      Version of Record online: 22 NOV 2013 | DOI: 10.1111/jnc.12529

      Read the full articleBeyond the mitochondrion: cytosolic PINK1 remodels dendrites through Protein Kinase A’ on doi: 10.1111/jnc.12494

  5. SHORT COMMUNICATIONS

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    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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      Rac1-mediated indentation of resting neurons promotes the chain migration of new neurons in the rostral migratory stream of post-natal mouse brain (pages 790–797)

      Takao Hikita, Akihisa Ohno, Masato Sawada, Haruko Ota and Kazunobu Sawamoto

      Version of Record online: 25 NOV 2013 | DOI: 10.1111/jnc.12518

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      New neurons generated in the ventricular-subventricular zone of the post-natal brain travel toward the olfactory bulb using a collective cell migration process called ‘chain migration.’ We found that chain-migrating neurons form an indentation in their cell body. Rac1 (Ras-related C3 botulinum toxin substrate 1) regulates the indentation in the resting neurons, which serve as a scaffold for the migrating neurons, thereby promoting chain migration non-cell-autonomously.

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      SUMOylation of MeCP2 is essential for transcriptional repression and hippocampal synapse development (pages 798–806)

      Ju Cheng, Min Huang, Ying Zhu, Yong-Juan Xin, Yun-Ke Zhao, Jian Huang, Jian-Xiu Yu, Wen-Hao Zhou and Zilong Qiu

      Version of Record online: 25 NOV 2013 | DOI: 10.1111/jnc.12523

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      The Methyl CpG binding protein 2 (MeCP2) is implicated in Rett syndrome and autism spectrum disorders. We showed that MeCP2 protein could be modified by SUMOylation and SUMOylation of MeCP2 is critical for its transcriptional regulation activity. Furthermore, we found that SUMOylation of MeCP2 plays a critical role in regulating synapse development in vitro and in vivo.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
    1. Gene Regulation & Genetics

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      Analysis of quantitative trait loci in mice suggests a role of Enoph1 in stress reactivity (pages 807–817)

      Alexander Barth, Andras Bilkei-Gorzo, Eva Drews, David M. Otte, Amalia Diaz-Lacava, Jeeva Varadarajulu, Christoph W. Turck, Thomas F. Wienker and Andreas Zimmer

      Version of Record online: 17 NOV 2013 | DOI: 10.1111/jnc.12517

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      Enoph1, an enzyme of the methionine salvage pathway involved in polyamine biosynthesis, was identified by QTL analysis as a candidate gene contributing to stress-sensitivity in a F2 population of mice derived from C57BL/6J × C3H/HeJ intercrosses. The parental strains express two different protein variants of Enoph1, show different Enoph1 expression levels, and have different brain spermidine levels. These findings suggest that Enoph1 modulates stress sensitivity in these strains.

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      Transcriptional regulation of human USP24 gene expression by NF-kappa B (pages 818–828)

      Ke Wang, Shengchun Liu, Juelu Wang, Yili Wu, Fang Cai and Weihong Song

      Version of Record online: 16 DEC 2013 | DOI: 10.1111/jnc.12626

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      Impairment of the ubiquitin proteasome system (UPS) has been implicated in neurodegenerative disorders. This report showed that the expression of human ubiquitin-specific protease 24 (USP24), a deubiquitinating enzyme of UPS, is tightly regulated by NFκB. The results suggest that dysregulation of NFκB-mediated USP24 expression may play a role in PD pathogenesis and modulating this process could have therapeutic potential.

    3. Signal Transduction & Synaptic Transmission

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      Murine dopaminergic Müller cells restore motor function in a model of Parkinson's disease (pages 829–840)

      Bernardo Stutz, Fabio Silva Lima da Conceição, Luís Eduardo Santos, Daniel Veloso Cadilhe, Renata L. Fleming, Mariana Acquarone, Patrícia F. Gardino, Ricardo A. de Melo Reis, Phillip W. Dickson, Peter R. Dunkley, Stevens Rehen, Jean-Christophe Houzel and Fernando G. de Mello

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12475

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      Müller cells are the main glial cells in the retina. When these cells are cultured in the absence of neurons, they spontaneously express proteins of the dopaminergic phenotype, including the enzymes tyrosine hydroxylase (TH), L-DOPA-decarboxylase (DDC) and the dopamine transport system (DAT). In this study, we show this phenomenon is observed with Müller cells obtained from different species, including primates, and address the therapeutic potential of these cells, using a mouse model of Parkinson's disease (PD). ‘Dopaminergic Müller cells’ synthesize dopamine and release most of this neurotransmitter to the extracellular space, constituting a natural dopaminergic ‘pump’. When transplanted to the striatum of PD mice, Müller cells decreased their apomorphine-induced rotational behavior and restored their overall motor functions, measured by rotarod and forelimb use asymmetry tests. Local restoration of dopaminergic signaling was also observed in grafted PD mice, by measuring striatum dopamine and its metabolite (DOPAC) levels (SB: 20µm).

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      Synaptic activity bidirectionally regulates a novel sequence-specific S-Q phosphoproteome in neurons (pages 841–851)

      Benjamin Siddoway, Hailong Hou, Hongtian Yang, Ronald Petralia and Houhui Xia

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12487

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      We discovered a novel phosphoproteome in neurons which is characterized by the phosphorylation of a specific motif (serine/threonine-glutamine, abbreviated as SQ). The SQ phosphoproteome is activated directly by synaptic activity-mediated Ca2+ influx from L-type calcium channels, and is localized to multiple subcellular domains, including dendritic shafts/spines. Substrates identified in this phosphoproteome exhibit diverse subcellular localizations and functions.

      Cover Image for this issue: doi: 10.1111/jnc.12545.

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      Thalamic synaptic transmission of sensory information modulated by synergistic interaction of adenosine and serotonin (pages 852–863)

      Ya-Chin Yang, Chun-Chang Hu, Chen-Syuan Huang and Pei-Yu Chou

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12499

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      Mimicking a scenario of the sleep-onset state, we found that wake-promoting serotonin and local somnogen adenosine interact to produce robust inhibition of synaptic transmission and reverse the short-term synaptic plasticity from depression to facilitation in the sensory thalamus, effects not achievable by one modulator alone but consistent with the expected electrophysiological characteristics at sleep. Thus, the relay of information through the thalamus can be finely tuned in a vigilance state-dependent context-specific manner by neuromodulators from both distant and local sources.

  7. HIGHLIGHTED ARTICLE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
    1. ORIGINAL ARTICLES

      Brain Development & Cell Differentiation
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      Beyond the mitochondrion: cytosolic PINK1 remodels dendrites through Protein Kinase A (pages 864–877)

      Ruben K. Dagda, Irene Pien, Ruth Wang, Jianhui Zhu, Kent Z. Q. Wang, Jason Callio, Tania Das Banerjee, Raul Y. Dagda and Charleen T. Chu

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12494

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      Mutations in PINK1 cause recessive Parkinson's disease, but the neuronal function(s) of the PINK1 protein remain elusive. We found that cytosolic PINK1 promotes neuronal differentiation in naïve cells, reversing dendritic shortening and cell death in Pink1−/− neurons, by increasing PKA activity and mitochondrial transport to dendrites. Release of processed PINK1 from healthy mitochondria may serve as a pro-differentiation signal in cortical and dopaminergic neurons.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12529

  8. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
    1. Brain Development & Cell Differentiation

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      HB-EGF affects astrocyte morphology, proliferation, differentiation, and the expression of intermediate filament proteins (pages 878–889)

      Till B. Puschmann, Carl Zandén, Isabell Lebkuechner, Camille Philippot, Yolanda de Pablo, Johan Liu and Milos Pekny

      Version of Record online: 26 NOV 2013 | DOI: 10.1111/jnc.12519

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      HB-EGF (heparin-binding EGF-like growth factor) was previously suggested to replace serum, a common and undefined component in primary astrocyte cultures. We show that both in standard 2D and in our newly developed Bioactive3D culture system, HB-EGF affects astrocyte morphology, proliferation, gene/protein expression and leads to partial de-differentiation of astrocytes. Thus, HB-EGF should only be used with caution as a serum replacement in astrocyte cultures.

    2. Neuroinflammation & Neuroimmunology

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      Increased toll-like receptor 4 in cerebral endothelial cells contributes to the astrocyte swelling and brain edema in acute hepatic encephalopathy (pages 890–903)

      Arumugam R. Jayakumar, Xiao Y. Tong, Kevin M. Curtis, Roberto Ruiz-Cordero, Maria T. Abreu and Michael D. Norenberg

      Version of Record online: 22 NOV 2013 | DOI: 10.1111/jnc.12516

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      Ammonia and inflammatory agents, such as lipopolysaccharide (LPS) or cytokines (CKs), activate the toll-like receptor 4 (TLR4) in endothelial cells (ECs) ultimately resulting in astrocyte swelling. TLR4 protein upregulation was detected in rat brain ECs in acute hepatic encephalopathy (AHE), whereas TLR4 knock-out mice exhibited a reduction in brain edema after AHE. These studies suggest that ECs significantly contribute to the astrocyte swelling/brain edema in AHE.

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      Cross-talk between IGF-1 and estrogen receptors attenuates intracellular changes in ventral spinal cord 4.1 motoneuron cells because of interferon-gamma exposure (pages 904–918)

      Sookyoung Park, Kenkichi Nozaki, Joshua A. Smith, James S. Krause and Naren L. Banik

      Version of Record online: 4 DEC 2013 | DOI: 10.1111/jnc.12520

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      Pro-inflammatory Th1 cytokine, IFN-γ induced cellular damage was investigated in VSC4.1 motoneurons. IFN-γ resulted in apoptosis and inflammatory changes in motoneurons. Apoptosis was mediated via up-regulation of calpain and subsequent cleavage of caspase-3. IGF-1 is suggested as potentially neuroprotective in motoneuron following cytokine exposure. Cellular protective effects of IGF-1 are mediated by cross-talk with ERα and ERβ in VSC4.1 motoneurons.

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      The role of tumor progression locus 2 protein kinase in glial inflammatory response (pages 919–926)

      Joshua Hirschhorn, Sangeeta Mohanty and Narayan R. Bhat

      Version of Record online: 21 NOV 2013 | DOI: 10.1111/jnc.12522

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      MAP kinase cascades including ERK, JNK, and p38 are involved in glial expression of inflammatory mediators. Recent studies identify TPL2, a newer member of MAP3K, as the major upstream activator of ERK in immune cells although essentially nothing is known about this kinase in glial cells. The studies presented define an important proinflammatory function of TPL2 pathway in these cells.

    5. Neuronal Plasticity & Behavior

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      CaMKII activity is essential for improvement of memory-related behaviors by chronic rivastigmine treatment (pages 927–937)

      Shigeki Moriguchi, Hideaki Tagashira, Yuzuru Sasaki, Jay Z. Yeh, Hiroyuki Sakagami, Toshio Narahashi and Kohji Fukunaga

      Version of Record online: 17 NOV 2013 | DOI: 10.1111/jnc.12510

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      We performed that whether chronic rivastigmine treatments improve hippocampal LTP in CA1 from CaMKIIα+/− mice. Rivastigmine treatments failed to improve LTP in CA1. In immunoblotting analysis, rivastigmine did not affect autophosphorylation of CaMKIIα (Thr-286) in CA1. Lack of rivastigmine effects in CaMKIIα+/− mice confirms that stimulation of CaMKII activity was critical for the rivastigmine-induced memory improvement.

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      Comparative effect of lurasidone and blonanserin on cortical glutamate, dopamine, and acetylcholine efflux: role of relative serotonin (5-HT)2A and DA D2 antagonism and 5-HT1A partial agonism (pages 938–949)

      Mei Huang, John J. Panos, Sunoh Kwon, Yoshihiro Oyamada, Lakshmi Rajagopal and Herbert Y. Meltzer

      Version of Record online: 14 NOV 2013 | DOI: 10.1111/jnc.12512

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      Abnormalities in dopaminergic, glutamatergic, gamma-aminobutyric acid (GABAergic), cholinergic, and noradrenergic activity in the medial prefrontal cortex and hippocampus have been implicated in the pathophysiology of the cognitive impairment in schizophrenia. Using in vivo microdialysis and UPLC-MS/MS assay method, the effect of multiple antipsychotics with different binding properties on the efflux of neurotransmitters including acetylcholine (ACh), dopamine (DA), and metabolites, serotonin, serine, glycine, glutamate (Glu) and GABA in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) have been studied in rats. Related mechanisms of receptors and neurotransmitter efflux have been discussed.

    7. Molecular Basis of Disease

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      Over-expression of an inactive mutant cathepsin D increases endogenous alpha-synuclein and cathepsin B activity in SH-SY5Y cells (pages 950–961)

      Donna Crabtree, Matthew Dodson, Xiaosen Ouyang, Michaël Boyer-Guittaut, Qiuli Liang, Mary E. Ballestas, Naomi Fineberg and Jianhua Zhang

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12497

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      Insufficiencies in the autophagy-lysosome pathway may contribute to neurodegenerative disease pathogenesis and progression. We found that a catalytically inactive mutant cathepsin D (D295N CD) decreases endogenous CD activity, similar to inhibition of endogenous CD activity by the addition of CD inhibitor, PepA, leads to accumulation of α-synuclein, without significant changes of overall autophagy activities. As accumulation of α-synuclein is a main pathological feature of Parkinson's disease (PD), this study further demonstrate a crucial role of CD activities in attenuation of synucleinopathies such as PD.

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      The putative multidrug resistance protein MRP-7 inhibits methylmercury-associated animal toxicity and dopaminergic neurodegeneration in Caenorhabditis elegans (pages 962–974)

      Natalia VanDuyn and Richard Nass

      Version of Record online: 25 NOV 2013 | DOI: 10.1111/jnc.12515

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      Methylmercury (MeHg) exposure is a risk factor for Parkinson's disease. Yet, the molecular basis for Hg transport and neurotoxicity is poorly defined. Our studies identify the first multidrug resistance protein that is targeted to dopamine (DA) neurons. We show that the transporter inhibits MeHg-associated accumulation of Hg, intracellular toxicant-associated stress response, and DA neurodegeneration. This model should facilitate the identification of molecular pathways and potential therapeutic targets involved in MeHg-associated dopamine neuron pathology. hsp = heat-shock protein.

  9. CORRIGENDUM

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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      Corrigendum (page 975)

      Version of Record online: 13 JUL 2011 | DOI: 10.1111/j.1471-4159.2011.07368.x

      This article corrects:

      Cyclo(His-Pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signalling

      Vol. 111, Issue 4, 956–966, Version of Record online: 7 SEP 2009

  10. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. SHORT COMMUNICATIONS
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    10. CORRIGENDUM
    11. ACKNOWLEDGEMENT OF REVIEWERS
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