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Journal of Neurochemistry

Cover image for Vol. 128 Issue 3

February 2014

Volume 128, Issue 3

Pages i–vii, 341–471

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL
    6. SHORT COMMUNICATION
    7. ORIGINAL ARTICLES
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      Issue Cover (February 2014)

      Version of Record online: 21 JAN 2014 | DOI: 10.1111/jnc.12536

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      Front cover: The image depicts multicolor epifluorescence and phase contrast photomicrograph of neurons (green), astrocytes (blue) and oligodendrocytes (red) derived from enriched rat subventricular zone derived multipotential neural precursors as described by Brazel and colleagues. J. Neurochem. 2014, vol. 128 (3), pp. 376–390.

      Read the full article on doi: 10.1111/jnc.12447

  2. Issue Information

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

      Version of Record online: 21 JAN 2014 | DOI: 10.1111/jnc.12537

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL
    6. SHORT COMMUNICATION
    7. ORIGINAL ARTICLES
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      In this Issue (pages iii–vii)

      Version of Record online: 21 JAN 2014 | DOI: 10.1111/jnc.12538

  4. EDITORIAL

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL
    6. SHORT COMMUNICATION
    7. ORIGINAL ARTICLES
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      Submitting a manuscript for peer review–integrity, integrity, integrity (pages 341–343)

      Sean P. Murphy, Christopher Bulman, Behnam Shariati, Laura Hausmann and on behalf of the ISN Publications Committee

      Version of Record online: 10 JAN 2014 | DOI: 10.1111/jnc.12644

  5. SHORT COMMUNICATION

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL
    6. SHORT COMMUNICATION
    7. ORIGINAL ARTICLES
    1. You have free access to this content
      Regulation of DNA methylation by ethanol induces tissue plasminogen activator expression in astrocytes (pages 344–349)

      Xiaolu Zhang, Handojo Kusumo, Amul J. Sakharkar, Subhash C. Pandey and Marina Guizzetti

      Version of Record online: 28 OCT 2013 | DOI: 10.1111/jnc.12465

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      We propose that ethanol, by decreasing DNMT-3a (DNA methyltransferase) levels and by inhibiting DNMT activity, reduces DNA methylation of the tissue plasminogen activator (tPA) promoter and leads to increased tPA mRNA and protein expression in astrocytes; tPA released is also increased by ethanol. As tPA promotes the degradation of neuritogenic extracellular matrix, the observed dysregulation of the epigenetic mechanism of DNA methylation in astyrocytes may be involved in ethanol-induced inhibition of astrocyte-mediated neuritogenesis.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL
    6. SHORT COMMUNICATION
    7. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Aβ40 modulates GABAA receptor α6 subunit expression and rat cerebellar granule neuron maturation through the ERK/mTOR pathway (pages 350–362)

      Xiao-Qin Zhan, Jin-Jing Yao, Dong-Dong Liu, Qianqian Ma and Yan-Ai Mei

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12471

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      In addition to its neurotoxic role in Alzheimer's disease, Aβ is known to play important physiological roles. Whether Aβ improves neuronal development and maturation remains elusive. Our results demonstrate that low concentrations of Aβ40 significantly increase the GABAA receptor α6 subunit expression and associated current in cerebellar granule neurons (CGNs) via the p75NTR and MEK/ERK pathway. Aβ also increases the thickness of the internal granule layer in APP−/− mice cerebellum. Our data provide new evidence for the role of Aβ40 in regulating the maturation of CGNs.

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      GABAA receptor transmembrane amino acids are critical for alcohol action: disulfide cross-linking and alkyl methanethiosulfonate labeling reveal relative location of binding sites (pages 363–375)

      Cecilia M. Borghese, Jessica A. Hicks, Daniel J. Lapid, James R. Trudell and R. Adron Harris

      Version of Record online: 28 OCT 2013 | DOI: 10.1111/jnc.12476

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      Alcohols modulate GABAA receptor function. The relative location of alcohol binding pockets in transmembrane domains was assessed by substituting critical amino acids with cysteines, and testing GABA responses and alcohol modulation before and after crosslinking double cysteine mutants and labeling single cysteine mutants. Lines show absence of crosslinking (red), and crosslinking that modified GABA responses (black) and alcohol modulation (grey).

    3. Brain Development & Cell Differentiation

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      Molecular features of neural stem cells enable their enrichment using pharmacological inhibitors of survival-promoting kinases (pages 376–390)

      Christine Y. Brazel, Abdulaziz A. Alaythan, Ryan J. Felling, Frances Calderon and Steven W. Levison

      Version of Record online: 10 OCT 2013 | DOI: 10.1111/jnc.12447

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      Neural stem cells resist death effectors, which contributes to their longevity. We demonstrate that primitive Subventricular Zone neural precursors express low levels of pro-apoptotic molecules and resist PI3K (PD98059) and ERK1/2 (LY-294002) inhibition. By contrast, progenitors expressed higher levels of cell-death signaling molecules. Using combinations of PI3K and ERK1/2 inhibitors, cultures highly enriched in tripotential neural precursors were produced.

      Cover Image for this issue: doi: 10.1111/jnc.12536.

    4. You have full text access to this OnlineOpen article
      A conserved sequence in calmodulin regulated spectrin-associated protein 1 links its interaction with spectrin and calmodulin to neurite outgrowth (pages 391–402)

      Mikayala D. A. King, Gareth W. Phillips, Paola A. Bignone, Nandini V. L. Hayes, Jennifer C. Pinder and Anthony J. Baines

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12462

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      Knockdown of the cytoskeletal protein CAMSAP1 using siRNA inhibited NGF-induced (nerve growth factor) neurite outgrowth from PC12 cells, and axon production by cerebellar granule cells in culture. This activity is linked to a spectrin- and Ca2+/calmodulin-binding region (CC1), since over-expression of isolated CC1 inhibited neurite production from PC12 cells. We previously showed that CAMSAP1 binds microtubules at the C-terminal CKK domain. Our data indicates CAMSAP1 is a cytoskeletal interconnector required for neurite and axon production.

    5. Molecular Basis of Disease

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      Transglutaminase 2 accelerates neuroinflammation in amyotrophic lateral sclerosis through interaction with misfolded superoxide dismutase 1 (pages 403–418)

      Miki Oono, Ayako Okado-Matsumoto, Akemi Shodai, Akemi Ido, Yasuyuki Ohta, Koji Abe, Takashi Ayaki, Hidefumi Ito, Ryosuke Takahashi, Naoyuki Taniguchi and Makoto Urushitani

      Version of Record online: 30 SEP 2013 | DOI: 10.1111/jnc.12441

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      A new role of transglutaminase 2 (TG2) in misfolded SOD1-linked neuroinflammation has been clarified. TG2 recognized and oligomerized only misfolded forms of SOD1, which robustly activated microglia, and induce the expression of proinflammatory molecules such as iNOS, IL-1β, and TNF-α. The inhibition of spinal cord TG2 of mutant SOD1 transgenic mice successfully suppressed neuroinflammation and delayed the progression.

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      A novel function for proSAAS as an amyloid anti-aggregant in Alzheimer's disease (pages 419–430)

      Akina Hoshino, Michael Helwig, Sina Rezaei, Casey Berridge, Jason L. Eriksen and Iris Lindberg

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12454

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      In this study, we describe a novel anti-aggregant function for the neuroendocrine protein, proSAAS. We found that proSAAS co-localizes with Aβ in Alzheimer's disease-affected brains, and co-immunoprecipitates with Aβ in brain extracts. In vitro, proSAAS efficiently prevents Aβ1–42 fibrillation, and also blocks Aβ1–42–mediated neurotoxicity. These results suggest that proSAAS may be a novel target for neurodegenerative disease therapy.

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      Changes in CNS cells in Hyperammonemic portal hypertensive rats (pages 431–444)

      Silvina Tallis, Laura R. Caltana, Pablo A. Souto, Amalia E. Delfante, Néstor R. Lago, Alicia Brusco and Juan C. Perazzo

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12458

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      Rats with pre-hepatic portal hypertension because of partial portal vein ligation afford a model of minimal hepatic encephalopathy that developed hyperammonemia. The cellular changes found here were similar to those described in ischemic conditions. Besides, a high expression of HIF-1α in cortical neurons was observed. It is likely that a hypoxia-like state is triggered via ammonia occupying the binding domain of HIF-1α and thereby preventing its degradation and inducing its stabilization, leading to the over-expression of P-gp and the Epo-R.

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      Corticosterone administration up-regulated expression of norepinephrine transporter and dopamine β-hydroxylase in rat locus coeruleus and its terminal regions (pages 445–458)

      Yan Fan, Ping Chen, Ying Li, Kui Cui, Daniel M. Noel, Elizabeth D. Cummins, Daniel J. Peterson, Russell W. Brown and Meng-Yang Zhu

      Version of Record online: 10 OCT 2013 | DOI: 10.1111/jnc.12459

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      Chronic stress and dysfunction of the noradrenergic system are etiologically related to depression. In an attempt to explore their interaction, we found that chronic ingestion of corticosterone (CORT) up-regulated expression of noradrenergic transporter (NET) and dopamine β-hydroxylase (DBH) in the locus coeruleus and its main projection regions, which may induce an increase in cellular norepinephrine concentration. This interaction may represent an adaptive action to stress for maintaining homeostasis.

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      Neuroprotective and anti-apoptotic effects of liraglutide on SH-SY5Y cells exposed to methylglyoxal stress (pages 459–471)

      Mohit K. Sharma, Jaishree Jalewa and Christian Hölscher

      Version of Record online: 28 OCT 2013 | DOI: 10.1111/jnc.12469

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      We investigated the neuroprotective properties of the GLP-1 analogue liraglutide in SH-SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro-survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro-apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.

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