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Journal of Neurochemistry

Cover image for Vol. 126 Issue 4

August 2013

Volume 126, Issue 4

Pages i–x, 425–549

  1. IN THIS ISSUE

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATIONS
    5. HIGHLIGHTED ARTICLES
    6. ORIGINAL ARTICLES
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      In this Issue (pages i–x)

      Version of Record online: 5 AUG 2013 | DOI: 10.1111/jnc.12367

  2. EDITORIAL HIGHLIGHT

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATIONS
    5. HIGHLIGHTED ARTICLES
    6. ORIGINAL ARTICLES
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      Guanosine behind the scene (pages 425–427)

      Francisco Ciruela

      Version of Record online: 1 JUL 2013 | DOI: 10.1111/jnc.12328

      Read the full articleGuanosine controls inflammatory pathways to afford neuroprotection of hippocampal slices under oxygen and glucose deprivation conditions’ on doi: 10.1111/jnc.12324

  3. SHORT COMMUNICATIONS

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATIONS
    5. HIGHLIGHTED ARTICLES
    6. ORIGINAL ARTICLES
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      The isolectin IB4 binds RET receptor tyrosine kinase in microglia (pages 428–436)

      Francesca Boscia, Carla Lucia Esposito, Antonella Casamassa, Vittorio de Franciscis, Lucio Annunziato and Laura Cerchia

      Version of Record online: 17 MAR 2013 | DOI: 10.1111/jnc.12209

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      The study demonstrates that isolectin IB4, commonly used as a microglial marker in the brain, binds to the glycosylated ectodomain of Ret tyrosine kinase receptor, the signaling component for the family ligands of the glial cell line-derived neurotrophic factor. Binding was observed in microglia under physiological and ischemic conditions, thus indicating Ret as one of the IB4-reactive glycoconjugate accounting for the IB4 stain in microglia.

  4. HIGHLIGHTED ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATIONS
    5. HIGHLIGHTED ARTICLES
    6. ORIGINAL ARTICLES
    1. ORIGINAL ARTICLES

      Signal Transduction & Synaptic Transmission
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      Guanosine controls inflammatory pathways to afford neuroprotection of hippocampal slices under oxygen and glucose deprivation conditions (pages 437–450)

      Tharine Dal-Cim, Fabiana K. Ludka, Wagner C. Martins, Charlise Reginato, Esther Parada, Javier Egea, Manuela G. López and Carla I. Tasca

      Version of Record online: 17 JUN 2013 | DOI: 10.1111/jnc.12324

      Thumbnail image of graphical abstract

      Guanosine (GUO) promotes neuroprotection against oxygen and glucose deprivation in hippocampal slices via a mechanism that involves modulation of adenosine receptors and activation of PI3K/AKT and MAPK/ERK. These signaling pathways are implicated in the prevention of mitochondrial membrane depolarization, reduction of oxidative stress, regulation of inflammation by inhibition of NF-κB and inducible nitric oxide synthase (iNOS), and the promotion of glutamate uptake. EAAT: excitatory amino acid transporter, ROS: reactive oxygen species.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12328.

  5. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATIONS
    5. HIGHLIGHTED ARTICLES
    6. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Choline transporter-like protein 4 (CTL4) links to non-neuronal acetylcholine synthesis (pages 451–461)

      Pingfang Song, Stephen S. Rekow, Corey-Ayne Singleton, Harmanjatinder S. Sekhon, Gregory A. Dissen, Minerva Zhou, Barbara Campling, Jon Lindstrom and Eliot R. Spindel

      Version of Record online: 25 JUN 2013 | DOI: 10.1111/jnc.12298

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      It is now well established that many non-neuronal cell types synthesize and secrete acetylcholine that acts as an autocrine or paracrine hormone. Although there are many similarities between neuronal and non-neuronal acetylcholine synthesis, there is a difference in choline transport for acetylcholine synthesis. Neurons must use the high affinity choline transporter CHT1, but many non-neuronal cells synthesize acetylcholine without CHT1. In this article, we show that non-neuronal cells utilize the choline transporter-like protein-4 (CTL4) for ACh synthesis.

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      Functional stoichiometry underlying KChIP regulation of Kv4.2 functional expression (pages 462–472)

      Kumud Kunjilwar, Yan Qian and Paul J. Pfaffinger

      Version of Record online: 9 JUN 2013 | DOI: 10.1111/jnc.12309

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      Mutations to the Kv4.2 potassium channel that disrupt KChIP binding act as dominant negative mutants to trap channels in intracellular membranes. This effect is due to the exposure of an N-terminal regulatory sequence (FERN, blue) on the potassium channel, and can be eliminated when this sequence is deleted.

    3. Neuroinflammation & Neuroimmunology

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      Systemic vaccination with anti-oligomeric monoclonal antibodies improves cognitive function by reducing Aβ deposition and tau pathology in 3xTg-AD mice (pages 473–482)

      Suhail Rasool, Hilda Martinez-Coria, Jessica W. Wu, Frank LaFerla and Charles G. Glabe

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/jnc.12305

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      We studied effect of immunotherapy of two sequence-independent non-fibrillar oligomer specific monoclonal antibodies on the cognitive function, amyloid load, and tau pathology in 3xTg-AD mice. Passive immunization with anti-oligomeric monoclonal antibodies effectively attenuates cognitive and pathological impairments in 3xTg-AD mice. These findings demonstrate the potential of using oligomer specific monoclonal antibodies as a therapeutic approach to prevent and treat Alzheimer's disease.

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      Identification of coronin-1a as a novel antibody target for clinically isolated syndrome and multiple sclerosis (pages 483–492)

      Myrthe Rouwette, Jean-Paul Noben, Jack Van Horssen, Bart Van Wijmeersch, Raymond Hupperts, Peter J. Jongen, Marcel M. Verbeek, Peter P. De Deyn, Piet Stinissen and Veerle Somers

      Version of Record online: 1 JUL 2013 | DOI: 10.1111/jnc.12335

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      Recently, we identified the mimotope UH-CIS6 as a novel antibody target for clinically isolated syndrome (CIS) and relapsing-remitting multiple sclerosis (RR-MS). By using a peptide ELISA, we detected a significantly increased frequency of anti-UH-CIS6 antibody reactivity in cerebrospinal fluid samples from CIS and RR-MS patients as compared with controls. Coronin-1a was identified and confirmed as the in vivo antibody target for UH-CIS6. Furthermore, coronin-1a was expressed by T cells and macrophages in MS brain. Together, our results demonstrate that coronin-1a is a novel antibody target for CIS and MS.

    5. Neuronal Plasticity & Behavior

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      Altered stress responsiveness and hypothalamic-pituitary-adrenal axis function in male rat offspring of socially isolated parents (pages 493–502)

      Maria Giuseppina Pisu, Anna Garau, Pierluigi Olla, Francesca Biggio, Cinzia Utzeri, Riccardo Dore and Mariangela Serra

      Version of Record online: 9 MAY 2013 | DOI: 10.1111/jnc.12273

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      Adult offspring of isolated rats exhibited an increased brain level of allopregnanolone, increased basal activity of the HPA axis, reduction of hypothalamic CRF and CRFR1 in the pituitary. There was also attenuation of corticosterone response by acute stress and up-regulation of GR expression in the hippocampus. In conclusion, a stressful experience before mating influence neuroendocrine signalling in the next generation.

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      Cellular distribution of AMPA receptor subunits and mGlu5 following acute and repeated administration of morphine or methamphetamine (pages 503–517)

      Amy A. Herrold, Amanda L. Persons and T. Celeste Napier

      Version of Record online: 18 JUN 2013 | DOI: 10.1111/jnc.12323

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      Chronic methamphetamine results in glutamate release and synaptic plasticity, likely involving AMPA receptors. Metabotropic glutamate receptor group 1 subtype 5 (mGlu5) activates striatal-enriched tyrosine phosphatase isoform 61 (STEP61) to internalize AMPARs. We reveal that repeated methamphetamine increased cell surface AMPAR subunits and decreased STEP61 levels in rat cortex; this change was not seen after mGlu5 antagonist treatment.

    7. Molecular Basis of Disease

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      Exposure to the cytokine EGF leads to abnormal hyperactivity of pallidal GABA neurons: implications for schizophrenia and its modeling (pages 518–528)

      Hidekazu Sotoyama, Hisaaki Namba, Satomi Chiken, Atsushi Nambu and Hiroyuki Nawa

      Version of Record online: 25 MAR 2013 | DOI: 10.1111/jnc.12223

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      Pallidal hyperactivity and hyperdopaminergic states found in a cytokine model for schizophrenia

      The indirect pathway of the basal ganglia circuit is implicated in cognition, motor coordination, learning and antipsychotic pharmacology. The activity of globus pallidus neurons in this pathway is markedly modulated by dopaminergic afferents. Perinatal expose to EGF induces pallidal hyperdopaminergic innervation and elevates their firing rates, resulting in increased GABA release. This pallidal dysfunction contributes to the neurobehavioral deficits of this animal model for schizophrenia.

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      Selective degeneration of dopaminergic neurons by MPP+ and its rescue by D2 autoreceptors in Drosophila primary culture (pages 529–540)

      Lyle Wiemerslage, Bradley J. Schultz, Archan Ganguly and Daewoo Lee

      Version of Record online: 24 MAR 2013 | DOI: 10.1111/jnc.12228

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      This study showed that a PD toxin MPP+ causes selective degeneration of dopaminergic (DA) neurons in a Drosophila primary culture. We also found that MPP+-mediated neurodegeneration was rescued by D2 agonists. Furthermore, activation of Drosophila D2 autoreceptors (D2Rauto) prevents MPP+ toxicity through suppression of DA neuronal excitability (or excitotoxicity).

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      Inflammation alters the expression of DMT1, FPN1 and hepcidin, and it causes iron accumulation in central nervous system cells (pages 541–549)

      Pamela Urrutia, Pabla Aguirre, Andrés Esparza, Victoria Tapia, Natalia P. Mena, Miguel Arredondo, Christian González-Billault and Marco T. Núñez

      Version of Record online: 3 APR 2013 | DOI: 10.1111/jnc.12244

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      Inflammation and iron accumulation are present in a variety of neurodegenerative diseases including Alzheimer's and Parkinson's disease. We analyzed the effects of the inflammatory cytokines TNF-α and Il-6 and of LPS on total cell iron content and on the expression and abundance of the iron transporters DMT1 and FPN1 in neurons, astrocytes, and microglia. Inflammatory stimuli increased expression of DMT1 in neurons, astrocytes, and microglia, induced the expression of hepcidin in astrocytes and microglia but not in neurons. Incubation with hepcidin transiently decreased the expression of FPN1 in the three cell types. The net result of these changes was increased iron accumulation in neurons and microglia but not in astrocytes. The findings establish a causal association between inflammation and iron accumulation in brain cells, presumably by changes in DMT1 and FPN1 expression and mediated in part by hepcidin.

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