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Journal of Neurochemistry

Cover image for Vol. 128 Issue 5

March 2014

Volume 128, Issue 5

Pages i–ix, 603–786

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. ORIGINAL ARTICLES
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      Issue Cover (March 2014)

      Version of Record online: 21 FEB 2014 | DOI: 10.1111/jnc.12542

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      Front cover: Shown is a frequency density heat map of the probe trial in a Morris water maze experiment with rats [control group from a KIBRA (KIdney/BRAin protein) viral knock-down experiment; n=20]. The color coding from red to yellow to green to blue to black indicates the probability of location of the animals during the probe trial run time (2 min) with red indicating the highest and black the lowest probability of location. The former platform location is in the upper left quadrant. J. Neurochem. 2014, vol. 128 (5), pp. 686–700.

      Read the full article on doi: 10.1111/jnc.12480

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. ORIGINAL ARTICLES
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      Issue Information (pages i–ii)

      Version of Record online: 21 FEB 2014 | DOI: 10.1111/jnc.12543

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. ORIGINAL ARTICLES
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      In this Issue (pages iii–ix)

      Version of Record online: 21 FEB 2014 | DOI: 10.1111/jnc.12544

  4. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. ORIGINAL ARTICLES
    1. Gene Regulation & Genetics

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      Phosphorylation of neuronal Lysine-Specific Demethylase 1LSD1/KDM1A impairs transcriptional repression by regulating interaction with CoREST and histone deacetylases HDAC1/2 (pages 603–616)

      Emanuela Toffolo, Francesco Rusconi, Leda Paganini, Marcello Tortorici, Simona Pilotto, Christopher Heise, Chiara Verpelli, Gabriella Tedeschi, Elisa Maffioli, Carlo Sala, Andrea Mattevi and Elena Battaglioli

      Version of Record online: 23 OCT 2013 | DOI: 10.1111/jnc.12457

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      LSD1-8a is a neurospecific splicing isoform of LSD1 that can be phosphorylated at a Thr residue coded by mini-exon E8a. Phosphorylation enhances LSD1-8a-driven neuronal maturation by hampering repressive potential on target morphogenic genes, which is achieved by causing CoREST/HDAC1/2 corepressor complex disassembly. In conclusion, interplay between alternative splicing (AS) and phosphorylation cooperate to set LSD1 repressive potential in the brain.

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      Expression of astrocytic genes coding for proteins implicated in neural excitation and brain edema is altered after acute liver failure (pages 617–627)

      Kiran K. Thumburu, Radha K. Dhiman, Rakesh K. Vasishta, Anuradha Chakraborti, Roger F. Butterworth, Elizabeth Beauchesne, Paul Desjardins, Sandeep Goyal, Navneet Sharma, Ajay Duseja and Yogesh Chawla

      Version of Record online: 14 NOV 2013 | DOI: 10.1111/jnc.12511

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      We investigated the gene expression of astrocytic proteins involved in astrocyte swelling causing brain edema in autopsied brain tissues of patients with acute liver failure. This study demonstrated loss of GFAP expression and up-regulation of AQP-4 protein expression leading to cerebral edema, and loss of EAAT-2 expression implicated in excitatory neurotransmission. These findings may provide new drug targets against CNS complications of acute liver failure.

    3. Bioenergetics & Metabolism

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      Differential effects of ethanol on regional glutamatergic and GABAergic neurotransmitter pathways in mouse brain (pages 628–640)

      Vivek Tiwari, Pandichelvam Veeraiah, Vaidyanathan Subramaniam and Anant Bahadur Patel

      Version of Record online: 14 NOV 2013 | DOI: 10.1111/jnc.12508

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      Depletion of ethanol and its effect on brain functions were measured using 1H and 1H-[13C]-NMR spectroscopy in conjunction with infusion of 13C-labeled substrates. Ethanol depletion from brain follows zero order kinetics. Ethanol perturbs level of glutamate, and the excitatory and inhibitory activity in mice brain.

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      The GLT-1 (EAAT2; slc1a2) glutamate transporter is essential for glutamate homeostasis in the neocortex of the mouse (pages 641–649)

      Lars Petter Bjørnsen, Mussie G. Hadera, Yun Zhou, Niels C. Danbolt and Ursula Sonnewald

      Version of Record online: 14 NOV 2013 | DOI: 10.1111/jnc.12509

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      Glutamate is the major excitatory neurotransmitter, and is inactivated by uptake via GLT-1 (EAAT2) and GLAST (EAAT1) transporters, while axon terminals in the neocortex only express GLT-1. To evaluate the role of GLT-1 in glutamate homeostasis, we used [1-13C]glucose and [1,2-13C]acetate injection and NMR spectroscopy. The results indicate that glutamine transport into neurons is not sufficient to replenish glutamate lost because of neurotransmission and that GLT-1 plays a role in glutamate homeostasis in the neocortex.

    5. Neuroinflammation & Neuroimmunology

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      Inflammation induces multinucleation of Microglia via PKC inhibition of cytokinesis, generating highly phagocytic multinucleated giant cells (pages 650–661)

      Tamara C. Hornik, Urte Neniskyte and Guy C. Brown

      Version of Record online: 30 OCT 2013 | DOI: 10.1111/jnc.12477

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      Inflammation resulted in the accumulation of multiple nuclei per cell in cultured microglia. This multinucleation was reversible and due to a PKC-dependent block of the last step of cell division. Multinucleate microglia were larger and had a greater capacity to phagocytose other cells, suggesting they might remove neurons in the brain.

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      Platelet activating factor induces transient blood-brain barrier opening to facilitate edaravone penetration into the brain (pages 662–671)

      Weirong Fang, Rui Zhang, Lan Sha, Peng Lv, Erxin Shang, Dan Han, Jie Wei, Xiaohan Geng, Qichuan Yang and Yunman Li

      Version of Record online: 14 NOV 2013 | DOI: 10.1111/jnc.12507

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      Platelet activating factor (PAF) transiently induces BBB dysfunction and increases BBB permeability, which may be due to vessel contraction and a temporary decline of regional cerebral blood flow (rCBF) triggered by PAF. More importantly, the PAF induced transient BBB opening facilitates neuroprotectant edaravone penetration into brain. The results of this study may provide a new approach to improve drug delivery into the brain.

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      Critical role of peripheral drug actions in experience-dependent changes in nucleus accumbens glutamate release induced by intravenous cocaine (pages 672–685)

      Ken T. Wakabayashi and Eugene A. Kiyatkin

      Version of Record online: 28 OCT 2013 | DOI: 10.1111/jnc.12472

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      Using high-speed amperometry with enzyme-based biosensors in freely moving rats, we show that initial intravenous cocaine induces rapid, transient glutamate (Glu) release in the Nac (Nucleus accumbens), rapidly becoming a stronger, two-component increase with subsequent injections. We show that the peripheral actions of cocaine, which precedes its direct central actions, play a critical role in experience-dependent alterations in Glu release, possibly contributing to cocaine addiction.

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      KIBRA (KIdney/BRAin protein) regulates learning and memory and stabilizes Protein kinase Mζ (pages 686–700)

      Angela Vogt-Eisele, Carola Krüger, Kerstin Duning, Daniela Weber, Robert Spoelgen, Claudia Pitzer, Christian Plaas, Gisela Eisenhardt, Annette Meyer, Gerhard Vogt, Markus Krieger, Eva Handwerker, Dirk Oliver Wennmann, Thomas Weide, Boris V. Skryabin, Matthias Klugmann, Hermann Pavenstädt, Matthew J. Huentelmann, Joachim Kremerskothen and Armin Schneider

      Version of Record online: 28 OCT 2013 | DOI: 10.1111/jnc.12480

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      KIBRA/WWC1 has been genetically associated with human episodic memory. KIBRA has been shown to be post-synaptically localized, but its function remained obscure. Here, we show that KIBRA shields PKMζ, a kinase previously linked to memory maintenance, from proteasomal degradation via direct interaction. KIBRA levels in the rodent hippocampus correlate closely both to spatial memory performance in rodents and to PKMζ levels. Our findings support a role for KIBRA in memory, and unveil a novel function for this protein.

      Cover Image for this issue: doi: 10.1111/jnc.12542.

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      Full-gestational exposure to nicotine and ethanol augments nicotine self-administration by altering ventral tegmental dopaminergic function due to NMDA receptors in adolescent rats (pages 701–712)

      Emily E. Roguski, Burt M. Sharp, Hao Chen and Shannon G. Matta

      Version of Record online: 15 NOV 2013 | DOI: 10.1111/jnc.12504

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      We hypothesized that concurrent gestational exposure to nicotine and ethanol would disrupt the control of VTA dopaminergic circuitry by NMDA receptors. Resulting in the augmented nicotine self-administration (SA) in adolescent offspring.

    10. Molecular Basis of Disease

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      Cathepsin E generates a sumoylated intracellular fragment of the cell adhesion molecule L1 to promote neuronal and Schwann cell migration as well as myelination (pages 713–724)

      David Lutz, Gerrit Wolters-Eisfeld, Melitta Schachner and Ralf Kleene

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12473

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      Cell adhesion molecule L1 regulates cellular responses in the developing and adult nervous system. L1 stimulation triggers sumoylation and cleavage of L1, thus generating the L1-70 fragment (1) which is cleaved by cathepsin E (2) yielding the L1-30 fragment that is imported to the nucleus (3), may bind to DNA and/or nuclear proteins (4), to regulate diverse cellular functions.

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      Regulation of the high-affinity choline transporter activity and trafficking by its association with cholesterol-rich lipid rafts (pages 725–740)

      Leah K. Cuddy, Warren Winick-Ng and Rebecca Jane Rylett

      Version of Record online: 4 NOV 2013 | DOI: 10.1111/jnc.12490

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      The sodium-coupled choline transporter CHT moves choline into cholinergic nerve terminals to serve as substrate for acetylcholine synthesis. We show for the first time that CHT is concentrated in cholesterol-rich lipid rafts, and decreasing membrane cholesterol significantly reduces both choline uptake activity and cell surface CHT protein levels. CHT association with cholesterol-rich rafts is critical for its function, and alterations in plasma membrane cholesterol could diminish cholinergic transmission by reducing choline availability for acetylcholine synthesis.

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      SCA14 mutation V138E leads to partly unfolded PKCγ associated with an exposed C-terminus, altered kinetics, phosphorylation and enhanced insolubilization (pages 741–751)

      Justyna Jezierska, Joachim Goedhart, Harm H. Kampinga, Eric A. Reits and Dineke S. Verbeek

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12491

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      Here, we show that the mutation V138E of the protein kinase C γ (PKCγ) C1B domain (PKCγ-V138E), which is implicated in spinocerebellar ataxia type 14, exhibits a partially unfolded C-terminus. This leads to unusually fast phorbol 12-myristate 13-acetate-induced membrane translocation and accumulation of phosphorylated PKCγ-V138E in the insoluble fraction, causing loss of the functional kinase. In contrast to general chaperones, coexpression of PKCγ's ‘natural chaperone’, PDK1 kinase, could rescue the PKCγ-V138E phenotype.

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      HIV increases the release of dickkopf-1 protein from human astrocytes by a Cx43 hemichannel-dependent mechanism (pages 752–763)

      Juan Andres Orellana, Juan Carlos Sáez, Michael Vander Lann Bennett, Joan Weinberger Berman, Susan Morgello and Eliseo Alberto Eugenin

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12492

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      Our studies demonstrated that HIV infection of astrocytes, despite minimal replication and a low number of infected cells, induces dysregulation of DKK1 secretion by a Cx43 hemichannel (HC)-dependent mechanism. Enhanced DKK1 secretion in response to HIV infection of glial cells compromised formation and stability of neuronal processes, similar to the synaptic compromise observed in HIV-infected individuals. In addition, analysis of human brain tissue sections obtained from encephalitic individuals also shows enhanced expression of DKK1 in astrocytes. Our data provide a novel mechanism by which HIV infection of glial cells participate in the pathogenesis of brain dysfunction observed in HIV-infected individuals. LRP5 = Low-density lipoprotein receptor-related protein 5.

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      Co-administration of betulinic acid and methamphetamine causes toxicity to dopaminergic and serotonergic nerve terminals in the striatum of late adolescent rats (pages 764–775)

      Bryan Killinger, Mrudang Shah and Anna Moszczynska

      Version of Record online: 3 DEC 2013 | DOI: 10.1111/jnc.12496

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      We report a synergistic neurotoxicity of betulinic acid (BA) and methamphetamine (METH) to monoaminergic terminals in the striatum of male late adolescent rats. BA contribution to the neurotoxicity is decreasing mitochondrial complex I whereas METH contribution is decreasing parkin and increasing brain concentration of BA. We propose that clinical use of BA in young male METH users can be neurotoxic.

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      Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat (pages 776–786)

      Michael R. Due, Jonghyuck Park, Lingxing Zheng, Michael Walls, Yohance M. Allette, Fletcher A. White and Riyi Shi

      Version of Record online: 13 NOV 2013 | DOI: 10.1111/jnc.12500

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      Following spinal cord injury (SCI), acrolein involvement in neuropathic pain is likely through direct activation and elevated levels of pro-nociceptive channel TRPA1. While acrolein elevation correlates with neuropathic pain, suppression of this aldehyde by hydralazine leads to an analgesic effect. Acrolein may serve as a novel therapeutic target for preclinical and clinical SCI to relieve both acute and chronic post-SCI neuropathic pain.

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