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Journal of Neurochemistry

Cover image for Vol. 125 Issue 4

May 2013

Volume 125, Issue 4

Pages 487–637

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
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      Mind the gut: secretion of α-synuclein by enteric neurons (pages 487–490)

      Stefan A. Grathwohl, Jennifer A. Steiner, Markus Britschgi and Patrik Brundin

      Version of Record online: 1 MAR 2013 | DOI: 10.1111/jnc.12191

      Read the full article ‘Activity-dependent secretion of alpha-synuclein by enteric neurons’ on doi: 10.1111/jnc.12131.

  2. REVIEW

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
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      Oxidative and nitrative alpha-synuclein modifications and proteostatic stress: implications for disease mechanisms and interventions in synucleinopathies (pages 491–511)

      Stefan Schildknecht, Hanne R. Gerding, Christiaan Karreman, Malte Drescher, Hilal A. Lashuel, Tiago F. Outeiro, Donato A. Di Monte and Marcel Leist

      Version of Record online: 19 MAR 2013 | DOI: 10.1111/jnc.12226

  3. HIGHLIGHTED ARTICLE

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
    1. SHORT COMMUNICATION

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      Activity-dependent secretion of alpha-synuclein by enteric neurons (pages 512–517)

      Sébastien Paillusson, Thomas Clairembault, Mandy Biraud, Michel Neunlist and Pascal Derkinderen

      Version of Record online: 15 JAN 2013 | DOI: 10.1111/jnc.12131

      Thumbnail image of graphical abstract

      Current evidence suggests that extracellular alpha-synuclein is critically involved in the spread of Parkinson's disease. As the enteric nervous system is affected early in Parkinson's disease, we undertook this research to investigate whether enteric neurons are capable of secreting alpha-synuclein. Using primary culture of enteric nervous system, we show that alpha-synuclein is physiologically secreted by enteric neurons in an activity-regulated manner. Our results reinforce the assumption that the enteric nervous system might be implicated in the pathophysiology of Parkinson's disease.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12191.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
    1. Gene Regulation & Genetics

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      Retinoids and glucocorticoids target common genes in hippocampal HT22 cells (pages 518–531)

      Julie Brossaud, Hélène Roumes, Marie-Pierre Moisan, Véronique Pallet, Anabelle Redonnet and Jean-Benoît Corcuff

      Version of Record online: 6 MAR 2013 | DOI: 10.1111/jnc.12192

      Thumbnail image of graphical abstract

      To better understand the mechanisms occurring during brain aging we studied genes altered by retinoids and glucocorticoids signalling in a hippocampal cell line. An interesting, but not unique, level of interaction is the altered transcription and translation of receptors involved in these pathways. Retinoic acid receptor β (RARβ) and glucocorticoid receptor (GR) are regulated by their own and reciprocal ligands, generating intricate and intertwined feedback loops.

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      Transient and rapid activation of Akt/GSK-3β and mTORC1 signaling by D3 dopamine receptor stimulation in dorsal striatum and nucleus accumbens (pages 532–544)

      Marie-Josèphe Salles, Denis Hervé, Jean-Michel Rivet, Sophie Longueville, Mark J. Millan, Jean–Antoine Girault and Clotilde Mannoury la Cour

      Version of Record online: 11 MAR 2013 | DOI: 10.1111/jnc.12206

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      Stimulation of D3, and possibly D2, dopamine receptors transiently activates Akt in the medium-size spiny neurons of the dorsal striatum and nucleus accumbens. Activated Akt can phosphorylate GSK-3β and, indirectly, several effectors of mTORC1: p70S6 kinase (p70S6K), ribosomal protein-S6 (rpS6), and eukaryotic initiation factor-4E binding protein-1 (4E-BP1). These pathways may underpin the actions of D3 receptors on diverse cerebral functions.

    3. Signal Transduction & Synaptic Transmission

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      GLAST/EAAT1-induced Glutamine release via SNAT3 in Bergmann glial cells: evidence of a functional and physical coupling (pages 545–554)

      Zila Martínez-Lozada, Alain M. Guillem, Marco Flores-Méndez, Luisa C. Hernández-Kelly, Carmelita Vela, Enrique Meza, Rossana C. Zepeda, Mario Caba, Angelina Rodríguez and Arturo Ortega

      Version of Record online: 11 MAR 2013 | DOI: 10.1111/jnc.12211

      Thumbnail image of graphical abstract

      A functional and physical coupling of glutamate uptake and glutamine release was characterized using cerebellar Bergmannglia cells. A time-dependent, GLAST-induced System N-mediated glutamine release could be demonstrated and a co-immunoprecipitation of GLAST and SNAT3 is described. Our results suggest that glial cells surrounding glutamatergic synapses may act as sensors of neuron-derived glutamate through their contribution to the turnover of this neurotransmitter.

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      Phasic-like stimulation of the medial forebrain bundle augments striatal gene expression despite methamphetamine-induced partial dopamine denervation (pages 555–565)

      Christopher D. Howard, Elissa D. Pastuzyn, Melissa L. Barker-Haliski, Paul A. Garris and Kristen A. Keefe

      Version of Record online: 1 APR 2013 | DOI: 10.1111/jnc.12234

      Thumbnail image of graphical abstract

      Methamphetamine (METH) neurotoxicity decreases striatal dopamine content. Associated with this dopamine depletion are deficits in phasic DA signaling, which is important for reward-based learning, and dysregulation of striatal gene expression. Here, using electrical stimulation of the medial forebrain bundle to activate dopamine neurons, we show that augmenting phasic DA signaling normalizes striatal gene expression, despite METH-induced partial DA depletions.

    5. Neuroinflammation & Neuroimmunology

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      Glial reactivity in resistance to methamphetamine-induced neurotoxicity (pages 566–574)

      Danielle M. Friend and Kristen A. Keefe

      Version of Record online: 17 MAR 2013 | DOI: 10.1111/jnc.12201

      Thumbnail image of graphical abstract

      We examined astrocyte and microglial reactivity in animals experiencing methamphetamine toxicity and in animals resistant to such toxicity. Animals experiencing toxicity showed activated microglia, whereas animals resistant to toxicity did not. Additionally, GFAP expression was similar whether an animal was experiencing toxicity or not, suggesting that astrocyte reactivity does not reflect acute METH-induced dopamine toxicity, whereas microglial reactivity does. DL, dorsolateral striatum; black bars: DM, dorsomedial striatum; white bars.

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      Astrocytes inhibit microglial surface expression of dendritic cell-related co-stimulatory molecules through a contact-mediated process (pages 575–587)

      Giselles Acevedo, Nischal K. Padala, Li Ni and G. M. Jonakait

      Version of Record online: 27 MAR 2013 | DOI: 10.1111/jnc.12221

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      Though often studied in isolation, microglia normally exist in an environment rich in neurons and other glia, notably astrocytes. Interactions with these other cell types are crucial for microglial function. With appropriate stimuli isolated microglia produce dendritic cell-related co-stimulatory molecules (e.g., CD40), but through a contact-mediated process, astrocytes promote the retention of those molecules in the ER preventing surface expression.

    7. Neuronal Plasticity & Behavior

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      Brain-derived neurotrophic factor, corticotropin-releasing factor, and hypothalamic neuronal histamine interact to regulate feeding behavior (pages 588–598)

      Koro Gotoh, Takayuki Masaki, Seiichi Chiba, Hisae Ando, Kansuke Fujiwara, Takanobu Shimasaki, Kimihiko Mitsutomi, Isao Katsuragi, Tetsuya Kakuma, Toshiie Sakata and Hironobu Yoshimatsu

      Version of Record online: 19 MAR 2013 | DOI: 10.1111/jnc.12213

      Thumbnail image of graphical abstract

      We have developed a working model of neuronal network via signaling between brain-derived neurotrophic factor (BDNF) and neuronal histamine. BDNF may act on histamine neurons in in the tuberomammillary nucleus (TMN) through corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus (PVN). Furthermore, neuronal histamine also stimulates BDNF neurons in the ventromedial nucleus (VMH) directly.

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      Stress-induced brain histone H3 phosphorylation: contribution of the intensity of stressors and length of exposure (pages 599–609)

      David Rotllant, Jordi Pastor-Ciurana and Antonio Armario

      Version of Record online: 11 MAR 2013 | DOI: 10.1111/jnc.12214

      Thumbnail image of graphical abstract

      Detailed knowledge about how the brain distinctly processes different types of emotional stressors is scarce. We demonstrate that phosphorylation of histone H3 (pH3) appears to be a good marker of stress-induced neuronal activation and show a more restricted pattern than classical marker such as c-fos. Detection of pH3 may help to more specifically identify brain areas and neurons important for the processing of emotional stressors.

    9. Molecular Basis of Disease

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      Substrate determinants in the C99 juxtamembrane domains differentially affect γ–secretase cleavage specificity and modulator pharmacology (pages 610–619)

      Solenne Ousson, Arman Saric, Aurelie Baguet, Christophe Losberger, Stephane Genoud, Francis Vilbois, Bruno Permanne, Ishrut Hussain and Dirk Beher

      Version of Record online: 18 JAN 2013 | DOI: 10.1111/jnc.12129

      Thumbnail image of graphical abstract

      Mutagenesis studies were conducted to explore γ-secretase cleavage specificity and modulation. Elongation of the distal juxtamembrane domain changes cleavage specificity. The K28E mutation at the proximal juxtamembrane domain changes γ-secretase cleavage specificity and modulator pharmacology. Thus, we have identified critical determinants in the proximal and distal juxtamembrane domains of the APP C99 substrate which differentially affect γ-secretase cleavage specificity and modulator pharmacology. Modulation of substrate binding could be a potential mechanism of action for γ-secretase modulators.

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      The octadecaneuropeptide ODN prevents 6-hydroxydopamine-induced apoptosis of cerebellar granule neurons through a PKC-MAPK-dependent pathway (pages 620–633)

      Hadhemi Kaddour, Yosra Hamdi, David Vaudry, Magalie Basille, Laurence Desrues, Jérôme Leprince, Hélène Castel, Hubert Vaudry, Marie-Christine Tonon, Mohamed Amri and Olfa Masmoudi-Kouki

      Version of Record online: 19 FEB 2013 | DOI: 10.1111/jnc.12140

      Thumbnail image of graphical abstract

      We proposed the following cascade for the neuroprotective effect of octadecaneuropeptide (ODN) against 6-OHDA-induced neuronal death: ODN provokes a stimulation of ERK phosphorylation, through a PKC-dependent mechanism. Activation of ERK counteracts the inhibition of Bcl-2 and the stimulation of the pro-apoptotic gene Bax induced by reactive oxygen species (ROS) formation and glutathione (GSH) depletion. These data may allow the development of new strategies for cerebral injury treatment.

  5. OBITUARY

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
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  6. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
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      Corrigendum (page 636)

      Version of Record online: 25 APR 2013 | DOI: 10.1111/jnc.12242

      This article corrects:

      A role for neuroserpin in neuron morphological development

      Vol. 121, Issue 4, 495–496, Version of Record online: 12 APR 2012

  7. RETRACTION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. HIGHLIGHTED ARTICLE
    5. ORIGINAL ARTICLES
    6. OBITUARY
    7. CORRIGENDUM
    8. RETRACTION
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      Retraction (page 637)

      Version of Record online: 25 APR 2013 | DOI: 10.1111/jnc.12241

      This article corrects:

      A role for neuroserpin in neuron morphological development

      Vol. 121, Issue 4, 495–496, Version of Record online: 12 APR 2012

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