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Journal of Neurochemistry

Cover image for Vol. 126 Issue 6

September 2013

Volume 126, Issue 6

Pages i–xii, 696–829

  1. IN THIS ISSUE

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
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      In this Issue (pages i–xii)

      Version of Record online: 6 SEP 2013 | DOI: 10.1111/jnc.12387

  2. EDITORIAL HIGHLIGHT

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
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      TMEM106B and frontotemporal lobar degeneration: can over-expression tell us how reductions are beneficial? (pages 696–698)

      Steven W. Barger

      Version of Record online: 22 JUL 2013 | DOI: 10.1111/jnc.12357

      Read the full article ‘TMEM106B p.T185S regulates TMEM106B protein levels: implications for frontotemporal dementia’ on doi:10.1111/jnc.12329.

  3. SHORT COMMUNICATION

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
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      Optineurin suppression causes neuronal cell death via NF-κB pathway (pages 699–704)

      Mayumi Akizuki, Hirofumi Yamashita, Kengo Uemura, Hirofumi Maruyama, Hideshi Kawakami, Hidefumi Ito and Ryosuke Takahashi

      Version of Record online: 17 JUN 2013 | DOI: 10.1111/jnc.12326

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      Among the genes for typical amyotrophic lateral sclerosis (ALS) phenotypes, optineurin (OPTN) is virtually the only gene in which a loss-of-function mutation is considered as the principal disease mechanism. We found that OPTN knockdown induced neuronal cell death via NF-κB activation. Furthermore, proapoptotic molecules such as p53 and Bax representing downstream targets of NF-κB are suggested to be involved in neuronal death.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
    1. Signal Transduction & Synaptic Transmission

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      Role of G-proteins in the effects of leptin on pedunculopontine nucleus neurons (pages 705–714)

      Paige Beck, Susan Mahaffey, Francisco J. Urbano and Edgar Garcia-Rill

      Version of Record online: 12 JUN 2013 | DOI: 10.1111/jnc.12312

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      Beck et al. investigated the effects of leptin on the intrinsic properties of neurons from the pedunculopontine nucleus (PPN). Leptin reduced the amplitude of voltage-gated sodium (INa) and hyperpolarization-activated cyclic nucleotide-gated HCN (IH) channels. These effects were antagonized by a leptin receptor (OB-R) antagonist and by the G-protein antagonist GDPβ.

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      The pre-synaptic Munc13-1 binds alcohol and modulates alcohol self-administration in Drosophila (pages 715–726)

      Joydip Das, Shiyu Xu, Satyabrata Pany, Ashley Guillory, Vrutant Shah and Gregg W. Roman

      Version of Record online: 10 JUN 2013 | DOI: 10.1111/jnc.12315

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      The pre-synaptic Mun13-1 protein is a critical regulator of synaptic vesicle fusion and may be involved in processes that lead to ethanol abuse and addiction. We studied its interaction with alcohol and identified Glu-582 as a critical residue for ethanol binding. Munc13-1 can functionally complement the Dunc13 haploinsufficient ethanol self-administration phenotype in Drosophila melanogaster, indicating that this protein participates in alcohol-induced behavioral plasticity.

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      Native STIM2 and ORAI1 proteins form a calcium-sensitive and thapsigargin-insensitive complex in cortical neurons (pages 727–738)

      Joanna Gruszczynska-Biegala and Jacek Kuznicki

      Version of Record online: 12 JUN 2013 | DOI: 10.1111/jnc.12320

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      We show in neuronal somata the formation of endogenous complexes of stromal interaction molecule 2 (STIM2) with ORAI1 calcium channels. Their number increased when intracellular Ca2+ concentrations were decreased by the Ca2+ chelator BAPTA-AM or a low-calcium medium (EGTA), but did not in the presence of thapsigargin (TG). We conclude that the small drop of Ca2+ level in endoplasmic reticulum, due to the decreased level of intracellular Ca2+, is sufficient to trigger STIM2-ORAI1 complex formation in a thapsigargin-insensitive manner.

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      Nesfatin-1 activates cardiac vagal neurons of nucleus ambiguus and elicits bradycardia in conscious rats (pages 739–748)

      G. Cristina Brailoiu, Elena Deliu, Andrei A. Tica, Joseph E. Rabinowitz, Douglas G. Tilley, Khalid Benamar, Walter J. Koch and Eugen Brailoiu

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12355

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      Our results indicate that nesfatin-1, one of the most potent feeding peptides, increases cytosolic Ca2+ by promoting Ca2+ influx via P/Q channels and depolarizes nucleus ambiguus neurons; both effects are Gi/o-mediated. In vivo studies indicate that microinjection of nesfatin-1 into nucleus ambiguus produces bradycardia in conscious rats. This is the first report that nesfatin-1 increases the parasympathetic cardiac tone.

    5. Brain Development & Cell Differentiation

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      Development of brainstem 5-HT1A receptor-binding sites in serotonin-deficient mice (pages 749–757)

      Caitlin A. Massey, Gloria Kim, Andrea E. Corcoran, Robin L. Haynes, David S. Paterson, Kevin J. Cummings, Susan M. Dymecki, George B. Richerson, Eugene E. Nattie, Hannah C. Kinney and Kathryn G. Commons

      Version of Record online: 10 JUN 2013 | DOI: 10.1111/jnc.12311

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      To elucidate the developmental relationship between serotonin (5-HT) levels and 5-HT1A receptors in the brainstem, we examined 5-HT1A binding in two 5-HT-deficient mouse models. In nuclei containing 5-HT neurons, 5-HT1A binding was decreased (autoreceptors), while binding was maintained in projection sites (heteroreceptors). Thus, brainstem 5-HT1A-heteroreceptor-binding sites do not appear developmentally sensitive to reduced brain 5-HT levels.

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      Insulin and IGF1 modulate turnover of polysialylated neural cell adhesion molecule (PSA–NCAM) in a process involving specific extracellular matrix components (pages 758–770)

      Hector J. Monzo, Thomas I. H. Park, Birger V. Dieriks, Deidre Jansson, Richard L. M. Faull, Mike Dragunow and Maurice A. Curtis

      Version of Record online: 5 AUG 2013 | DOI: 10.1111/jnc.12363

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      Neural cell adhesion molecules (NCAMs) are critically involved in cell differentiation and migration. Polysialylation (PSA)/desialylation of NCAMs switches their functional interaction mode and, in turn, migration and differentiation. We have found that the desialylation process of PSA–NCAM occurs via endocytosis, induced by collagen-IV and blocked by insulin-like growth factor (IGF1) and insulin, suggesting a novel association between PSA–NCAM, IGF1/insulin and brain/tumour plasticity.

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      microRNA-181a is involved in insulin-like growth factor-1-mediated regulation of the transcription factor CREB1 (pages 771–780)

      Yang Liu, Zhao Zhao, Fan Yang, Yimei Gao, Jian Song and Yu Wan

      Version of Record online: 6 AUG 2013 | DOI: 10.1111/jnc.12370

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      microRNAs (miRNAs) regulate gene expression at the post-transcriptional level and are involved in the central nervous system development. Here, we demonstrate that miR-181a can inhibit the expression of the transcription factor CREB1 by specifically targeting its mRNA 3′UTR and inhibit the development of hippocampus neurons. Repressed expression of miR-181a is involved in IGF-1-mediated up-regulation of CREB1 in vivo and in vitro. These findings indicate that miR-181a could be a potential target for preventing neurodegenerative diseases.

  5. HIGHLIGHTED ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
    1. ORIGINAL ARTICLES

      Molecular Basic of Disease
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      TMEM106B p.T185S regulates TMEM106B protein levels: implications for frontotemporal dementia (pages 781–791)

      Alexandra M. Nicholson, NiCole A. Finch, Aleksandra Wojtas, Matt C. Baker, Ralph B. Perkerson III, Monica Castanedes-Casey, Linda Rousseau, Luisa Benussi, Giuliano Binetti, Roberta Ghidoni, Ging-Yuek R. Hsiung, Ian R. Mackenzie, Elizabeth Finger, Bradley F. Boeve, Nilüfer Ertekin-Taner, Neill R. Graff-Radford, Dennis W. Dickson and Rosa Rademakers

      Version of Record online: 1 JUL 2013 | DOI: 10.1111/jnc.12329

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      We studied the p.T185S TMEM106B genetic variant previously implicated in frontotemporal dementia with TAR DNA binding protein 43 pathology caused by progranulin mutations. Our cell culture studies provide evidence that the protective S185 isoform is degraded more rapidly than T185 TMEM106B, potentially due to differences in glycosylation. These findings suggest that low TMEM106B levels might protect against FTLD-TDP in these patients.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12357.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
    1. Molecular Basic of Disease

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      A HuD-ZBP1 ribonucleoprotein complex localizes GAP-43 mRNA into axons through its 3′ untranslated region AU-rich regulatory element (pages 792–804)

      Soonmoon Yoo, Hak H. Kim, Paul Kim, Christopher J. Donnelly, Ashley L. Kalinski, Deepika Vuppalanchi, Michael Park, Seung J. Lee, Tanuja T. Merianda, Nora I. Perrone-Bizzozero and Jeffery L. Twiss

      Version of Record online: 30 APR 2013 | DOI: 10.1111/jnc.12266

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      We have recently found that over-expression of GAP-43 using an axonally targeted construct with the 3′UTRs of GAP-43 promoted elongating growth of axons, while restricting the mRNA to the cell body with the 3′UTR of γ-actin had minimal effect on axon length. In this study, we show that the ARE in GAP-43′s 3′UTR is responsible for localization of GAP-43 mRNA into axons and is sufficient for GAP-43 protein's role in elongating axonal growth.

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      Autophagy alleviates neurodegeneration caused by mild impairment of oxidative metabolism (pages 805–818)

      Ya Meng, Yue Yong, Guang Yang, Hanqing Ding, Zhiqin Fan, Yifen Tang, Jia Luo and Zun-Ji Ke

      Version of Record online: 9 JUN 2013 | DOI: 10.1111/jnc.12268

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      Autophagy is neuroprotective in response to thiamine deficiency (TD)-induced neuronal death. TD caused neuronal damage and induced the formation of autophagosome, and increased the expression of autophagy-related proteins. Autophagy sequestered damaged and dysfunctional organelles/protein, and transported them to lysosomes for degradation/recycling. This process provided nutrients for injured neurons. Wortmannin and knockdown of Beclin1 inhibited autophagy, and exacerbated TD-induced cell death, while activation of autophagy by rapamycin offered protection against TD neurotoxicity.

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      Citicoline (CDP-choline) increases Sirtuin1 expression concomitant to neuroprotection in experimental stroke (pages 819–826)

      Olivia Hurtado, Macarena Hernández-Jiménez, Juan G. Zarruk, María I. Cuartero, Iván Ballesteros, Guadalupe Camarero, Ana Moraga, Jesús M. Pradillo, María A. Moro and Ignacio Lizasoain

      Version of Record online: 13 MAY 2013 | DOI: 10.1111/jnc.12269

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      Sirtuin 1 (SIRT1) is implicated in a wide range of cellular functions. Regarding stroke, there is no direct evidence. We have demonstrated that citicoline increases SIRT1 protein levels in brain concomitantly to neuroprotection. Citicoline fails to reduce infarct volume in Sirt1-/- mice. Our findings suggest that therapeutic strategies acting on SIRT1 may be useful in the treatment of stroke.

  7. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. HIGHLIGHTED ARTICLES
    7. ORIGINAL ARTICLES
    8. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content

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