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Journal of Neurochemistry

Cover image for Vol. 125 Issue 2

April 2013

Volume 125, Issue 2

Pages 172–327

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. HIGHLIGHTED ARTICLE
    6. ORIGINAL ARTICLES
    1. You have free access to this content
      A gliovascular idea for the white matter repair? (pages 172–174)

      Berislav V. Zlokovic

      Version of Record online: 27 FEB 2013 | DOI: 10.1111/jnc.12174

      Read the full article ‘High-mobility group box 1 from reactive astrocytes enhances the accumulation of endothelial progenitor cells in damaged white matter’ on doi: 10.1111/jnc.12120.

  2. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. HIGHLIGHTED ARTICLE
    6. ORIGINAL ARTICLES
    1. You have free access to this content
      Deficiency of G3BP1, the stress granules assembly factor, results in abnormal synaptic plasticity and calcium homeostasis in neurons (pages 175–184)

      Sophie Martin, Latifa Zekri, Alexandra Metz, Tangui Maurice, Karim Chebli, Michel Vignes and Jamal Tazi

      Version of Record online: 6 MAR 2013 | DOI: 10.1111/jnc.12189

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      The RNA-binding protein G3BP (Ras-GAP SH3-domain-binding Protein) is an essential component of stress granules, characterized by arrested translation. We developed a knockout (KO) mouse showing a role for G3BP1 in synaptic conduction in the hippocampus and calcium homeostasis, and in motor coordination. These KO mice provide a good model for neurodegenerative diseases involving stress granules formation.

  3. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. HIGHLIGHTED ARTICLE
    6. ORIGINAL ARTICLES
    1. Gene Regulation & Genetics

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      Stress-induced changes in gene expression of urocortin 2 and other CRH peptides in rat adrenal medulla: involvement of glucocorticoids (pages 185–192)

      Andrej Tillinger, Regina Nostramo, Richard Kvetnansky, Lidia Serova and Esther L. Sabban

      Version of Record online: 5 FEB 2013 | DOI: 10.1111/jnc.12152

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      We found that gene expression of urocortin 2 (Ucn2) is not only the most abundant of CRH family members in adrenal medulla but also that stress triggers an enormous induction of Ucn2 mRNA levels. The stress-triggered release of CRH and rise of glucocorticoids is important for Ucn2 gene expression. Elevated Ucn2 can modulate adrenomedullary function in autocrine/paracrine fashion, with possible endocrine effect.

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      Dopamine D2 receptor activation leads to an up-regulation of glial cell line–derived neurotrophic factor via Gβγ-Erk1/2-dependent induction of Zif268 (pages 193–204)

      Somayeh Ahmadiantehrani and Dorit Ron

      Version of Record online: 27 FEB 2013 | DOI: 10.1111/jnc.12178

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      Glial cell line–derived neurotrophic factor (GDNF) is essential for the survival, development, and function of dopaminergic neurons. The mechanisms governing its expression are largely unknown. We found that dopamine, via a D2R-Gβγ-ERK1/2 pathway, up-regulates the Zif268 transcription factor, which directly associates with the GDNF promoter to drive GDNF expression. Our findings suggest that this pathway may be targeted for the treatment of Parkinson's disease and drug addiction, as well as the enhancement of learning and memory processes.

    3. Signal Transduction & Synaptic Transmission

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      Chondroitin sulfate, a major component of the perineuronal net, elicits inward currents, cell depolarization, and calcium transients by acting on AMPA and kainate receptors of hippocampal neurons (pages 205–213)

      Marcos Maroto, José-Carlos Fernández-Morales, Juan Fernando Padín, José C. González, Jesús M. Hernández-Guijo, Eulalia Montell, Josep Vergés, Antonio M. G. de Diego and Antonio G. García

      Version of Record online: 14 FEB 2013 | DOI: 10.1111/jnc.12159

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      Chondroitin sulfate (CS) may not play a simple role as a major component of proteoglycans (CSPGs) of extracellular matrix and perineural net (ECM/PNN). We present evidence to suggest that free CS, coming from CSPGs degradation, could play a relevant functional role in the regulation of hippocampal neurotransmission and synaptic plasticity, through the activation of an inward Na+-dependent current (ICS) that causes membrane depolarization (Em) and a cytosolic Ca2+ transient.

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      Permissive role of Cdc2 activity induced from astrocytes in neurite outgrowth (pages 214–224)

      In Ae Chang, Ku-Birm Kwon, Yang-Chun Park and Uk Namgung

      Version of Record online: 13 FEB 2013 | DOI: 10.1111/jnc.12163

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      We found that Cdc2 was strongly induced from reactive astrocytes after spinal cord injury. In long-term cultured astrocytes, Cdc2 phosphorylation of vimentin and activation of β3 integrin were associated with enhanced neurite outgrowth of co-cultured neurons. Our results suggest that astrocytes may attain permissiveness for regenerative responses via Cdc2 pathway activation.

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      BDNF prevents NMDA-induced toxicity in models of Huntington's disease: the effects are genotype specific and adenosine A2A receptor is involved (pages 225–235)

      Alberto Martire, Rita Pepponi, Maria Rosaria Domenici, Antonella Ferrante, Valentina Chiodi and Patrizia Popoli

      Version of Record online: 27 FEB 2013 | DOI: 10.1111/jnc.12177

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      BDNF prevents NMDA-induced toxicity in models of Huntington's disease: the effects are genotype specific and adenosine A2A receptor is involved

      We observed that BDNF, similar to adenosine A2A receptors' (A2ARs) stimulation, reduces NMDA-induced toxicity in Huntington's disease (HD) models, whereas increases it in wild-type preparations. In both genotypes, BDNF actions are prevented by A2AR blockade, confirming that A2ARs, directly and by activating TrkBRs, profoundly affect NMDAR functioning. These findings may have very important implications for the neuroprotective potential of both BDNF and A2AR ligands in HD.

    6. Bioenergetics & Metabolism

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      Glucose metabolism down-regulates the uptake of 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (6-NBDG) mediated by glucose transporter 1 isoform (GLUT1): theory and simulations using the symmetric four-state carrier model (pages 236–246)

      Mauro DiNuzzo, Federico Giove, Bruno Maraviglia and Silvia Mangia

      Version of Record online: 27 FEB 2013 | DOI: 10.1111/jnc.12164

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      In this study, we used the four-state carrier model for brain GLUT1 to examine whether cellular glucose metabolism can be inferred from the accumulation of the fluorescent glucose analogue 6-NBDG, which is increasingly employed for indirect determination of glucose transport and utilization in neurons and astrocytes. However, our findings show that the relation between 6-NBDG uptake and glucose transport and utilization configures antiport not symport of the two substrates.

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      Regional registration of [6-14C]glucose metabolism during brain activation of α-syntrophin knockout mice (pages 247–259)

      Nancy F. Cruz, Kelly K. Ball, Stanley C. Froehner, Marvin E. Adams and Gerald A. Dienel

      Version of Record online: 6 MAR 2013 | DOI: 10.1111/jnc.12166

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      Substantial lactate release from activated brain contradicts the notion that lactate shuttling provides major fuel. α-Syntrophin knockout mice were used to determine whether loss of the polarized localization of aquaporin4 (AQP4) at astrocytic endfeet influences lactate washout during sensory stimulation. Autoradiographic assays revealed greater retention of [14C]glucose metabolites in brain, suggesting that endfoot water fluxes contribute to metabolite washout via perivascular-lymphatic drainage.

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      Formaldehyde metabolism and formaldehyde-induced stimulation of lactate production and glutathione export in cultured neurons (pages 260–272)

      Ketki Tulpule, Michaela C. Hohnholt and Ralf Dringen

      Version of Record online: 24 FEB 2013 | DOI: 10.1111/jnc.12170

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      Cultured cerebellar granule neurons efficiently metabolize exogenously applied formaldehyde which results in cellular and extracellular accumulation of formate. Formaldehyde exposure accelerates glycolysis, possibly due to inhibition of cytochrome c oxidase of the mitochondrial respiration chain by cellular formate, and stimulates glutathione (GSH) export via the multidrug resistance protein (Mrp) 1. These alterations could play a role in formaldehyde-induced neurotoxicity.

  4. HIGHLIGHTED ARTICLE

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. HIGHLIGHTED ARTICLE
    6. ORIGINAL ARTICLES
    1. Neuronal Plasticity & Behavior

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      High-mobility group box 1 from reactive astrocytes enhances the accumulation of endothelial progenitor cells in damaged white matter (pages 273–280)

      Kazuhide Hayakawa, Nobukazu Miyamoto, Ji Hae Seo, Loc-Duyen D. Pham, Kyu-Won Kim, Eng H. Lo and Ken Arai

      Version of Record online: 28 DEC 2012 | DOI: 10.1111/jnc.12120

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      Beyond cell-cell signaling within the brain, crosstalk between brain and blood cells is now proposed as an important facet for brain recovery. In this study, we demonstrate that astrocyte-derived HMGB1 is an important mediator for attracting circulating endothelial progenitor cells (EPSc) into damaged white matter. Our findings may provide an important mechanism for the dynamic crosstalk between brain and circulating blood cells.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12174.

  5. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. HIGHLIGHTED ARTICLE
    6. ORIGINAL ARTICLES
    1. Neuronal Plasticity & Behavior

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      nAChR-induced octopamine release mediates the effect of nicotine on a startle response in Drosophila melanogaster (pages 281–290)

      Nicolás Fuenzalida-Uribe, Rodrigo C. Meza, Hernán A. Hoffmann, Rodrigo Varas and Jorge M. Campusano

      Version of Record online: 4 MAR 2013 | DOI: 10.1111/jnc.12161

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      Octopamine (Oct) is a biogenic amine that plays a central role in the generation of behaviors in invertebrates. Using a new Drosophila brain preparation we show that α-bungarotoxin-sensitive nAChRs induce a fast, transient, dose-dependent efflux of endogenous Oct. We further show that the nAChR-induced Oct release is involved in the nicotine impairment of a mechanically-induced startle response.

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      The nicotine-mediated decline in l-dopa-induced dyskinesias is associated with a decrease in striatal dopamine release (pages 291–302)

      Tanuja Bordia, J. Michael McIntosh and Maryka Quik

      Version of Record online: 3 MAR 2013 | DOI: 10.1111/jnc.12179

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      l-dopa-induced dyskinesias are a debilitating side effect of Parkinson's disease therapy that may arise because of excessive dopaminergic activity. Our previous studies showed that nicotine treatment reduced dyskinesias in Parkinsonian animal models. This study suggests that nicotine improves dyskinesias by reducing nicotinic receptor expression and function, that is, dopamine release.

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      Enhanced hippocampus-dependent memory and reduced anxiety in mice over-expressing human catalase in mitochondria (pages 303–313)

      Reid H. J. Olsen, Lance A. Johnson, Damian G. Zuloaga, Charles L. Limoli and Jacob Raber

      Version of Record online: 6 MAR 2013 | DOI: 10.1111/jnc.12187

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      The role of reactive oxygen species and mitochondria in cognition of healthy individuals is relatively understudied. Adult mice over-expressing mitochondrial catalase (MCAT) show reduced measures of anxiety in the elevated zero maze (left) and enhanced hippocampus-dependent memory in the contextual fear conditioning test (right an water maze). Measures of oxidative stress did not differ between the groups. Thus, catalase over-expression might be sufficient to cause these effects.

    4. Molecular Basis of Disease

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      Loss of DJ-1 protein stability and cytoprotective function by Parkinson's disease-associated proline-158 deletion (pages 314–327)

      Emmy H. Rannikko, Louise Buur Vesterager, Jafar H. A. Shaik, Stephanie S. Weber, Elena M. Cornejo Castro, Karina Fog, Poul H. Jensen and Philipp J. Kahle

      Version of Record online: 15 JAN 2013 | DOI: 10.1111/jnc.12126

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      DJ-1wt inhibits ASK1 activation by preferably binding to its N-terminal domain in presence of oxidative stress. The unstable and dimerization-defective DJ-1P158Δ mutant interacts with ASK1 also under normal conditions; the binding site may differ from the one for the wild-type. This leads to decreased inhibition of ASK1 activation and hence decreased cytoprotection.

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