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Journal of Neurochemistry

Cover image for Vol. 124 Issue 6

March 2013

Volume 124, Issue 6

Pages 747–897

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. CORRIGENDUM
    6. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
  2. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. CORRIGENDUM
    6. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
      Mitochondrial localization of the Forkhead box class O transcription factor FOXO3a in brain (pages 749–756)

      Aurelien Caballero-Caballero, Tobias Engel, Jaime Martinez-Villarreal, Amaya Sanz-Rodriguez, Patrick Chang, Mark Dunleavy, Claire M. Mooney, Eva M. Jimenez-Mateos, Clara K. Schindler and David C. Henshall

      Article first published online: 15 JAN 2013 | DOI: 10.1111/jnc.12133

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      ‘Mitochondrial localization of the Forkhead box class O transcription factor FOXO3a in brain’

      We identify a novel subcellular localization for FOXO3a, a transcription factor involved in development, life-span, and apoptosis control. We show that FOXO3a resides in mitochondria in the mouse, rat, and human hippocampus, where it may target mitochondrial DNA. We also found changes to levels of mitochondrial FOXO3a in experimental seizure models and human epilepsy. These findings open a new area of research on FOXO3a.

  3. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. CORRIGENDUM
    6. ACKNOWLEDGEMENT OF REVIEWERS
    1. Gene Regulation & Genetics

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      Transcriptional analysis of rat photoreceptor cells reveals daily regulation of genes important for visual signaling and light damage susceptibility (pages 757–769)

      Stefanie Kunst, Tanja Wolloscheck, Philip Hölter, Alexander Wengert, Markus Grether, Carsten Sticht, Veronika Weyer, Uwe Wolfrum and Rainer Spessert

      Article first published online: 13 JAN 2013 | DOI: 10.1111/jnc.12089

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      The aim of this study was to gain a better understanding of the daily adjustment of photoreceptor cells. Genes with an impact on photoreceptor function and survival were identified to be under daily and circadian regulation in photoreceptor cells. A hypothetical concept is proposed in which the transcriptional regulation of photoreceptor function is regulated not only by a circadian clock but also directly by ambient illumination (via Grk1 and Pgc-1α). Clock- and illumination-dependent regulation of gene expression may contribute to adaptation of visual function and, possibly, survival of photoreceptor cells.

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      Comprehensive gene expression analyses of the rat prefrontal cortex after oxysterol treatment (pages 770–781)

      Sau-Yeen Loke, Kazuhiro Tanaka and Wei-Yi Ong

      Article first published online: 4 FEB 2013 | DOI: 10.1111/jnc.12142

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      The present study was carried out using microarray analyses, to elucidate global gene expression changes in the rat prefrontal cortex after oxysterol treatment. These findings provide insight into possible molecular mechanisms through which oxysterols could exert a pathophysiological effect in the brain.

    3. Signal Transduction & Synaptic Transmission

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      The α-subunit of the trimeric GTPase Go2 regulates axonal growth (pages 782–794)

      Jens Baron, Christian Blex, Astrid Rohrbeck, Sivarama Krishna Rachakonda, Lutz Birnbaumer, Gudrun Ahnert-Hilger and Irene Brunk

      Article first published online: 3 FEB 2013 | DOI: 10.1111/jnc.12123

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      Go1α is known to be involved in axonal growth, whereas Go2α had not been investigated in this respect so far. Active Go2α interacts with Rap1GAP. Cerebral Rap1GTP levels and axonal growth and branching are enhanced in Go2α−/− mice, when compared with wild-type mice. Go2α regulates axonal growth, most likely via Rap1GAP and Rap1.

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      Neuron-type specific cannabinoid-mediated G protein signalling in mouse hippocampus (pages 795–807)

      Frauke Steindel, Raissa Lerner, Martin Häring, Sabine Ruehle, Giovanni Marsicano, Beat Lutz and Krisztina Monory

      Article first published online: 13 FEB 2013 | DOI: 10.1111/jnc.12137

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      Neuron-type specific cannabinoid-mediated G protein signalling in mouse hippocampus

      In this article we describe cell-type specific cannabinoid G protein signalling in the mouse hippocampus. Though most of hippocampal CB1 receptors can be found in the GABAergic neurons, they host only one third of the cannabinoid-activated G proteins. Glutamatergic neurons that express only the minority of CB1 accommodate two thirds of cannabinoid-activated G proteins.

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      Striatal CB1 and D2 receptors regulate expression of each other, CRIP1A and delta opioid systems (pages 808–820)

      Lawrence C. Blume, Caroline E. Bass, Steven R. Childers, George D. Dalton, David C. S. Roberts, Jasmine M. Richardson, Ruoyu Xiao, Dana E. Selley and Allyn C. Howlett

      Article first published online: 31 JAN 2013 | DOI: 10.1111/jnc.12139

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      Schematic representation of changes in striatal proteins following knockdown of CB1R or D2R. Striatal knockdown of either CB1R or D2R decreased expression of the alternative receptor, and reduced [35S]GTPγS binding, phosphoERK, pDYN and pENK expression, but increased DOR1. CB1R or D2R knockdown increased CRIP1a, which evoked similar responses. These studies identify a functional interaction between these receptor systems in vivo.

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      The P2X7 receptor as a route for non-exocytotic glutamate release: dependence on the carboxyl tail (pages 821–831)

      Chiara Cervetto, Susanna Alloisio, Daniela Frattaroli, Maria Chiara Mazzotta, Marco Milanese, Paola Gavazzo, Mario Passalacqua, Mario Nobile, Guido Maura and Manuela Marcoli

      Article first published online: 3 FEB 2013 | DOI: 10.1111/jnc.12143

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      P2X7 receptors as a route for non-exocytotic glutamate efflux

      P2X7 receptors trigger Ca2+-dependent exocytotic glutamate release, but also function as a route for non-exocytotic glutamate release. The P2X7 receptor's function for non-exocytotic glutamate efflux was dependent on the receptor C-tail and involved the juxtamembrane cysteine-rich motif of the tail. The finding should be relevant to understand the impact of naturally occurring P2X7 variants on glutamatergic transmission in health and disease.

    7. Neuronal Plasticity & Behavior

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      Male-specific alteration in excitatory post-synaptic development and social interaction in pre-natal valproic acid exposure model of autism spectrum disorder (pages 832–843)

      Ki Chan Kim, Pitna Kim, Hyo Sang Go, Chang Soon Choi, Jin Hee Park, Hee Jin Kim, Se Jin Jeon, Ike Campomayor dela Pena, Seol-Heui Han, Jae Hoon Cheong, Jong Hoon Ryu and Chan Young Shin

      Article first published online: 3 FEB 2013 | DOI: 10.1111/jnc.12147

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      Prenatal VPA exposure induces male inclined autistic symptoms including impaired social interactions and seizure susceptibility in rat fetus. These gender-specific impairments of VPA-exposed rats, which are similar to human autistic patients, may provide experimental models to elucidate the gender-dependent symptoms and molecular mechanisms in anti-social disorders including ASD, especially focusing on the development of excitatory/inhibitory nervous systems and synapses.

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      Age-dependent dystonia in striatal Gγ7 deficient mice is reversed by the dopamine D2 receptor agonist pramipexole (pages 844–854)

      Keita Sasaki, Tatsuro Yamasaki, Idowu O. Omotuyi, Masayoshi Mishina and Hiroshi Ueda

      Article first published online: 19 FEB 2013 | DOI: 10.1111/jnc.12149

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      Gγ7 KO mice exhibited age-dependent motor dysfunction such as clasping reflex and motor incoordination without a significant loss of striatal projection neurons. The behavioral dyskinesia in Gγ7 KO mice was reversed during chronic administration of the D2R agonist pramipexole.

    9. Molecular Basis of Disease

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      Omega-3 fatty acid eicospentaenoic acid attenuates MPP+-induced neurodegeneration in fully differentiated human SH-SY5Y and primary mesencephalic cells (pages 855–868)

      Dirk W. Luchtman, Qingjia Meng, Xiaofeng Wang, Di Shao and Cai Song

      Article first published online: 13 JAN 2013 | DOI: 10.1111/jnc.12068

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      Omega-3 fatty acids may be effective as a potential therapeutic compound against Parkinson's disease (PD), but research is still in its infancy. Herein, we show that omega-3 fatty acid eicosapentaenoic acid (EPA) prevents neurodegeneration induced by Parkinsonian toxin MPP+ in SH-SY5Y cells and primary mesencephalic neurons. Several experiments show that mechanisms of protection are antioxidant, anti-inflammatory, neurotrophic, and antiapoptotic action.

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      Suppression of pain-related behavior in two distinct rodent models of peripheral neuropathy by a homopolyarginine-conjugated CRMP2 peptide (pages 869–879)

      Weina Ju, Qi Li, Yohance M. Allette, Matthew S. Ripsch, Fletcher A. White and Rajesh Khanna

      Article first published online: 20 JAN 2013 | DOI: 10.1111/jnc.12070

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      Chronic neuropathic pain remains a worldwide medical problem with few effective therapies. Drugs targeting calcium channels are in clinical use as first-line treatments for alleviation of neuropathic pain. However, targeting these channels can lead to serious complications. Here, we report that a peptide derived from CRMP2 – a modulator of calcium channels, offers problem-free pain relief in rodent models of neuropathic pain.

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      Over-expression of heat shock factor 1 phenocopies the effect of chronic inhibition of TOR by rapamycin and is sufficient to ameliorate Alzheimer's-like deficits in mice modeling the disease (pages 880–893)

      Anson Pierce, Natalia Podlutskaya, Jonathan J. Halloran, Stacy A. Hussong, Pei-Yi Lin, Raquel Burbank, Matthew J. Hart and Veronica Galvan

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12080

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      Chronic inhibition of TOR or overexpression of HSF1, the master regulator of the heat shock response reduce amyloid, upregulate chaperones, and improve cognitive function in mice modeling Alzheimer's disease (AD). We propose that a mechanism by which chronic inhibition of TOR alleviates cognitive deficits involves preventing a decline in proteostasis that critically enables pathogenic processes of AD in aged brains.

  4. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. CORRIGENDUM
    6. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
  5. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. CORRIGENDUM
    6. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content

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