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Journal of Neurochemistry

Cover image for Vol. 127 Issue 1

October 2013

Volume 127, Issue 1

Pages 1–148

  1. NEWS AND ISN

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

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
    1. You have free access to this content
      Is exercise-in-a-bottle likely to proffer new insights into Alzheimer's disease? (pages 4–6)

      Sónia C. Correia, George Perry, Rudy Castellani and Paula I. Moreira

      Version of Record online: 24 SEP 2013 | DOI: 10.1111/jnc.12406

      Read the full article ‘Lactate administration reproduces specific brain and liver exercise-related changes’ on doi: 10.1111/jnc.12394.

  3. REVIEW

    1. Top of page
    2. NEWS AND ISN
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. ORIGINAL ARTICLES
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      Formaldehyde in brain: an overlooked player in neurodegeneration? (pages 7–21)

      Ketki Tulpule and Ralf Dringen

      Version of Record online: 14 JUL 2013 | DOI: 10.1111/jnc.12356

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      The neurotoxin formaldehyde is an environmental pollutant that is also generated during normal brain metabolism. The levels of formaldehyde in brain increase with age and in some neurodegenerative disorders. As excess formaldehyde accelerates glycolysis and glutathione export in neural cells, formaldehyde-induced alterations in brain metabolism and oxidative stress may contribute to the pathological progression of neurodegenerative disorders.

  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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      Binding of the repressor complex REST-mSIN3b by small molecules restores neuronal gene transcription in Huntington's disease models (pages 22–35)

      Paola Conforti, Chiara Zuccato, Germano Gaudenzi, Alessandro Ieraci, Stefano Camnasio, Noel J. Buckley, Cesare Mutti, Franco Cotelli, Alessandro Contini and Elena Cattaneo

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12348

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      Dysregulation of REST and its target genes have been implicated in Huntington's disease. We have coupled structured-based virtual screening approaches to biological assays and selected molecules that interfere with the repressor complex REST-mSIN3b. In particular, at the non-toxic dose, compound C91 is able to increase neuronal gene transcription and to reverse low Bdnf mRNA levels in HD models.

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      Promoter-like sequences regulating transcriptional activity in neurexin and neuroligin genes (pages 36–47)

      Fabian Runkel, Astrid Rohlmann, Carsten Reissner, Stefan-Martin Brand and Markus Missler

      Version of Record online: 20 AUG 2013 | DOI: 10.1111/jnc.12372

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      Neurexins and neuroligins constitute large families of synaptic cell-surface molecules that play essential roles in neurotransmission and are linked to autism spectrum disorders and schizophrenia. To better understand their gene regulation, we analyze putative promoter regions for transcriptional activity. Expression involves the brain-specific regulator MeCP2 and methylation frequency, suggesting an unexpected pathway for regulating their distribution, splicing or activity-dependent plasticity.

    3. Signal Transduction & Synaptic Transmission

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      Amyloid precursor proteins are constituents of the presynaptic active zone (pages 48–56)

      Melanie Laßek, Jens Weingarten, Ulf Einsfelder, Peter Brendel, Ulrike Müller and Walter Volknandt

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12358

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      We deciphered the precise subcellular localization of APP at the nerve terminal. We demonstrate that APP and its family members, APLP1 and APLP2, are constituents of the presynaptic active zone, albeit virtually absent in synaptic vesicles (SV). Our findings open new avenues for understanding the physiological role of the mature APP proteins at synaptic contacts, implying a function in the physiology of neurotransmitter release.

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      Arrestin-dependent but G-protein coupled receptor kinase-independent uncoupling of D2-dopamine receptors (pages 57–65)

      Jeremy Celver, Meenakshi Sharma, Vaidehi Thanawala, J. Christopher Octeau and Abraham Kovoor

      Version of Record online: 29 JUL 2013 | DOI: 10.1111/jnc.12359

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      The classical model for the uncoupling and desensitization of G-protein coupled receptors (GPCRs) involves the phosphorylation of the agonist-bound receptor by G protein coupled receptor kinases (GRK), followed by the binding of arrestin to the GRK phosphorylated agonist-activated receptor. We reconstituted D2-dopamine receptor (D2R) signaling in Xenopus oocytes to show that arrestin-mediated uncoupling of D2R from associated G proteins (Gαβγ) occurs independently of GRKs.

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      AMP-activated protein kinase counteracts brain-derived neurotrophic factor-induced mammalian target of rapamycin complex 1 signaling in neurons (pages 66–77)

      Yuta Ishizuka, Naomasa Kakiya, Lee A. Witters, Noriko Oshiro, Tomoaki Shirao, Hiroyuki Nawa and Nobuyuki Takei

      Version of Record online: 29 JUL 2013 | DOI: 10.1111/jnc.12362

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      Here, we report that growth factor-induced mTORC1 activity is dependent on glucose sufficiency, but not on amino acids in neurons. The mechanism underlying this phenomenon is AMP-activated protein kinase (AMPK) activation. AMPK activation inhibits BDNF-induced mTORC1 activity through TSC2 and raptor.

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      Depolarization-induced suppression of a glycinergic synapse in the superior olivary complex by endocannabinoids (pages 78–90)

      Barbara Trattner, Sarah Berner, Benedikt Grothe and Lars Kunz

      Version of Record online: 5 AUG 2013 | DOI: 10.1111/jnc.12369

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      We report retrograde endocannabinoid modulation of synaptic strength in auditory brainstem nuclei of the Mongolian gerbil. Utilising electrophysiological recordings and immunohistochemistry, we found endocannabinoid-dependent suppression of excitatory and inhibitory glycinergic currents in the same neurone types. We propose that retrograde endocannabinoid signalling contributes to adapting inputs to sound environment in the time period around the onset of functional hearing.

    7. Bioenergetics & Metabolism

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      Lactate administration reproduces specific brain and liver exercise-related changes (pages 91–100)

      Lezi E, Jianghua Lu, J. Eva Selfridge, Jeffrey M. Burns and Russell H. Swerdlow

      Version of Record online: 26 AUG 2013 | DOI: 10.1111/jnc.12394

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      In mice, exercise induces liver peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) mRNA, increases gluconeogenesis, but otherwise minimally affects respiration infrastructure. Brain PGC-1-related co-activator (PRC) mRNA, mitochondrial DNA (mtDNA), and vascular endothelial growth factor A (VEGF-A) mRNA increase, whereas tumor necrosis factor alpha (TNF-α) mRNA decreases. Lactate injection reproduces some, but not all, of these effects. Exercise-generated lactate, therefore, likely mediates some exercise-associated liver and brain effects.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12406.

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      Polyglucosan neurotoxicity caused by glycogen branching enzyme deficiency can be reversed by inhibition of glycogen synthase (pages 101–113)

      Or Kakhlon, Hava Glickstein, Naomi Feinstein, Yan Liu, Otto Baba, Tatsuo Terashima, Hasan Orhan Akman, Salvatore DiMauro and Alexander Lossos

      Version of Record online: 9 MAY 2013 | DOI: 10.1111/jnc.12277

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      Knockdown of glycogen branching enzyme in neurons led to accumulation of an insoluble form of glycogen called polyglucosan, to apoptosis and to activation of glycogen synthase. These effects were reversed by glycogen synthase inhibition through starvation and rapamycin treatments, suggesting a potential therapeutic value of glycogen synthase inhibition for treating glycogen storage disorders.

    9. Molecular Basis of Disease

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      Novel systemically active galanin receptor 2 ligands in depression-like behavior (pages 114–123)

      Indrek Saar, Jaanus Lahe, Kent Langel, Johan Runesson, Kristin Webling, Jaak Järv, Jussi Rytkönen, Ale Närvänen, Tamas Bartfai, Kaido Kurrikoff and Ülo Langel

      Version of Record online: 31 MAY 2013 | DOI: 10.1111/jnc.12274

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      We utilize several chemical modifications to increase in vivo usability of peptide-based ligands, acting upon CNS. Accordingly, we introduce a series of novel systemically active galanin analogues, with modest preferential binding towards GalR2, and demonstrate their ability to attenuate depression-like behavior via brain GalR2 in different mouse models of depression.

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      PrPC regulates epidermal growth factor receptor function and cell shape dynamics in Neuro2a cells (pages 124–138)

      Franc Llorens, Patricia Carulla, Ana Villa, Juan M. Torres, Puri Fortes, Isidre Ferrer and José A. del Río

      Version of Record online: 28 MAY 2013 | DOI: 10.1111/jnc.12283

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      In this study, we analyzed the PrPC-dependent gene expression signature of neuroblastoma (N2a) cells after transient acute up-regulation and down-regulation of PrPC. We demonstrate that PrPC plays roles in proliferation and neuritogenesis through modulation of EGFR activity. This approach will give new insights into the molecular mechanisms by which PrPC regulates key cellular functions in cell physiology.

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      PI3Kγ contributes to MEK1/2 activation in oxidative glutamate toxicity via PDK1 (pages 139–148)

      Jong Seong Ha, Ki-Sun Kwon and Sung Sup Park

      Version of Record online: 4 AUG 2013 | DOI: 10.1111/jnc.12364

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      Glutamate induces extracellular H2O2 generation by NADPH oxidase 4 (Nox4), leading to cell death in neurons. Our experiments, using siRNAs and chemical inhibitors, showed the PI3Kγ-PDK1-MEK axis but not Akt1, mTOR, or S6K to be involved in the glutamate-induced H2O2 generation and the subsequent toxicity in neurons.

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