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Journal of Neurochemistry

Cover image for Vol. 124 Issue 4

February 2013

Volume 124, Issue 4

Pages 431–580

  1. NEWS AND ISN

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
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      NEWS AND ISN (page 431)

      Article first published online: 28 JAN 2013 | DOI: 10.1111/jnc.12134

  2. EDITORIAL HIGHLIGHT

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
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      Gangliosides as regulators of cell signaling: ganglioside-protein interactions or ganglioside-driven membrane organization? (pages 432–435)

      Sandro Sonnino, Laura Mauri, Maria G. Ciampa and Alessandro Prinetti

      Article first published online: 28 JAN 2013 | DOI: 10.1111/jnc.12088

      Read the full article ‘Involvement of gangliosides in the process of Cbp/PAG phosphorylation by Lyn in developing cerebellar growth cones’ on doi: 10.1111/jnc.12040.

  3. REVIEW

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
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      Neuromodulation: selected approaches and challenges (pages 436–453)

      Vladimir Parpura, Gabriel A. Silva, Peter A. Tass, Kevin E. Bennet, M. Meyyappan, Jessica Koehne, Kendall H. Lee and Russell J. Andrews

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12105

  4. ORIGINAL ARTICLES

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
    1. Gene Regulation & Genetics

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      Targeted deletion of the antisilencer/enhancer (ASE) element from intron 1 of the myelin proteolipid protein gene (Plp1) in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination (pages 454–465)

      Glauber B. Pereira, Fanxue Meng, Neriman T. Kockara, Baoli Yang and Patricia A. Wight

      Article first published online: 21 DEC 2012 | DOI: 10.1111/jnc.12092

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      Removal of the antisilencer/enhancer (ASE) element from Plp1 intron 1 shows that it is essential for robust activation of Plp1-lacZ constructs in oligodendroglial cell lines, but dispensable for activation of the native gene in mouse during development and remyelination. Perhaps the ASE does not function in vivo, or its loss can be compensated for by other regulatory elements in Plp1.

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      RACK1 identified as the PCBP1-interacting protein with a novel functional role on the regulation of human MOR gene expression (pages 466–477)

      Pranjal Nahar-Gohad, Hamidah Sultan, Ysabella Esteban, Alyda Stabile and Jane L. Ko

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12100

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      RACKing up a New Regulatory Role: The human MOR gene is regulated by many factors, including PCBP1. Using the two-hybrid screening study with a human brain cDNA library, the authors identified RACK1 and showed that it physically interacts with PCBP1 mainly via WD7 domain and regulates MOR expression. This report adds to the variety of RACK1 interactions and provides further information how cells regulate MOR expression.

    3. Signal Transduction & Synaptic Transmission

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      Seipin regulates excitatory synaptic transmission in cortical neurons (pages 478–489)

      Shunhui Wei, Stephanie Li-Ying Soh, Wenjie Qiu, Wulin Yang, Cheyenne Jia-Yan Seah, Jing Guo, Wei-Yi Ong, Zhiping P. Pang and Weiping Han

      Article first published online: 27 DEC 2012 | DOI: 10.1111/jnc.12099

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      Seipin, an ER protein with high-level expression in brain, is implicated in a broad spectrum of motoneuron diseases. Seipin specifically regulates excitatory postsynaptic currents (EPSCs) as knockdown (KD) of Seipin results in significantly reduced AMPA receptor (AMPA-R)-mediated currents. Moreover, Seipin KD causes decreased total and surface AMPA-R levels. We conclude that Seipin regulates synaptic transmission through a postsynaptic mechanism.

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      Differential association of postsynaptic signaling protein complexes in striatum and hippocampus (pages 490–501)

      Anthony J. Baucum II, Abigail M. Brown and Roger J. Colbran

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12101

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      The organization of postsynaptic signaling proteins in different brain regions is poorly understood. We found that the protein phosphatase 1 binding protein, spinophilin, and CaMKII associated more robustly with each other and with the GluN2B NMDAR subunit in a striatal extrasynaptic fraction compared to the hippocampus. These data demonstrate brain region- and subcellular fraction-specific differences in synaptic protein organization.

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      Neuregulin 1 up-regulates the expression of nicotinic acetylcholine receptors through the ErbB2/ErbB3-PI3K-MAPK signaling cascade in adult autonomic ganglion neurons (pages 502–513)

      Han-Gyu Kim, Choong-Ku Lee, Sung-Min Cho, Kum Whang, Byong-Ho Cha, Ju-Hyun Shin, Ki-Hak Song and Seong-Woo Jeong

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12109

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      Neuregulin 1 (NRG1) is critical for formation of the autonomic nicotinic synapseduring development. However, the functional role of NRG1 in adult autonomic neurons remains unknown. We found NRG1-mediated up-regulation of the nicotinic acetylcholine receptor via the ErbB2/ErbB3-PI3K-MAPK signaling in MPG neurons of adult rat. This finding suggests that NRG1 is also required for maintenance of adult autonomic nicotinic synapse.

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      Involvement of gangliosides in the process of Cbp/PAG phosphorylation by Lyn in developing cerebellar growth cones (pages 514–522)

      Naoko Sekino-Suzuki, Kohei Yuyama, Toshiaki Miki, Mizuho Kaneda, Hidenori Suzuki, Naomasa Yamamoto, Tadashi Yamamoto, Chitose Oneyama, Masato Okada and Kohji Kasahara

      Article first published online: 14 JAN 2013 | DOI: 10.1111/jnc.12040

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      Functional association of gangliosides with Csk-binding protein in cerebellar growth cone rafts

      This work aimed to study the role of gangliosides in the nervous system. We demonstrated that anti-ganglioside antibody co-immunoprecipitated Csk-binding protein (Cbp) and Src family kinase Lyn from cerebellum, and treatment of primary cerebellar cultures with anti-ganglioside antibody induced Lyn activation and tyrosine 314 phosphorylation of Cbp in growth cone rafts. This suggests that gangliosides are platforms of transmembrane signaling by Lyn and Cbp.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12134.

    7. Neuroinflammation & Neuroimmunology

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      Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice (pages 523–535)

      Jiwon Yang, Hye-na Ahn, Minsun Chang, Purnima Narasimhan, Pak H. Chan and Yun Seon Song

      Article first published online: 28 DEC 2012 | DOI: 10.1111/jnc.12111

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      Our result showed that complement component 3 (C3) activation was down-regulated by antioxidant after cerebral ischemia, and was neuroprotective in mice model. Oxidative stress was highly related to C3activation after stroke, and C3 knock-down reduced ROS in primary neurons after hypoxia. An antioxidant that is able to inhibit C3 may offer the new strategy for therapeutic approaches in stroke.

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      15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) protects neurons from oxidative death via an Nrf2 astrocyte-specific mechanism independent of PPARγ (pages 536–547)

      Renée E. Haskew-Layton, Jimmy B. Payappilly, Hongbin Xu, Steffany A. L. Bennett and Rajiv R. Ratan

      Article first published online: 3 JAN 2013 | DOI: 10.1111/jnc.12107

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      15-Deoxy-Δ12,14-Prostaglandin J2 (15d-PGJ2) is an endogenous electrophile that activates the transcription factors PPARγ and Nrf2. Astrocytic 15d-PGJ2 protects neurons from depletion of the antioxidant glutathione via an Nrf2-dependent, PPARγ-independent mechanism. 15d-PGJ2 is a candidate endogenous modulator of the antioxidant transcription factor Nrf2 in astrocytes. This work delineates the integral non-cell autonomous neuroprotective role of 15d-PGJ2.

    9. Molecular Basis of Disease

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      Differential expression of parvalbumin in neonatal phencyclidine-treated rats and socially isolated rats (pages 548–557)

      Sanne S. Kaalund, Jesper Riise, Brian V. Broberg, Katrine Fabricius, Anna S. Karlsen, Thomas Secher, Niels Plath and Bente Pakkenberg

      Article first published online: 25 DEC 2012 | DOI: 10.1111/jnc.12061

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      Decreased parvalbumin (PV) expression is a pathophysiological hallmark of schizophrenia associated with cognitive deficits. Using a stereological approach we report a loss of parvalbumine-positive interneurons in the prefrontal cortex of the neonatal PCP rat model. The translational aspect favours the use of the model in future studies aiming at unravelling the role of parvalbumin-positive interneurons in cortical dysfunction.

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      Novel crosstalk between ERK MAPK and p38 MAPK leads to homocysteine-NMDA receptor-mediated neuronal cell death (pages 558–570)

      Ranjana Poddar and Surojit Paul

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12102

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      Hyperhomocysteinemia is an independent risk factor for neurological disorders. We report here that homocysteine-NMDA receptor mediated neuronal death involves a novel interplay between ERK and p38 MAPK where activation of p38 MAPK is downstream of and dependent on ERK MAPK. The direct regulatory role of ERK MAPK in p38 MAPK activation reveals a previously unidentified cellular mechanism for neuronal cell death.

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      Transient exposure to echinacoside is sufficient to activate Trk signaling and protect neuronal cells from rotenone (pages 571–580)

      Min Zhu, Chuanzhen Lu and Wenwei Li

      Article first published online: 26 DEC 2012 | DOI: 10.1111/jnc.12103

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      Neurotrophic activity of echinacoside

      The most significant challenge of therapeutic use of neurotrophins in treating neurodegenerative diseases is their delivery into the central nervous system. Here we reported that echinacoside, a small natural compound, elicits potent neuroprotection by activating Trk signaling. Since echinacoside is able to cross the blood–brain barrier freely, it may have a promising potential in neurodegenerative diseases treatment.

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