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Journal of Neurochemistry

Cover image for Vol. 127 Issue 5

December 2013

Volume 127, Issue 5

Pages 575–732

  1. PREFACE

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. You have free access to this content
      Molecular imaging and its applications: visualization beyond imagination (pages 575–577)

      Stephen R. Williams, Laura Hausmann and Jörg B. Schulz

      Version of Record online: 30 OCT 2013 | DOI: 10.1111/jnc.12445

  2. EDITORIAL HIGHLIGHT

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. You have free access to this content
      Early impairment in brain metabolism detected by MR spectroscopy antedates structural changes in mouse models of spinocerebellar ataxias (pages 578–579)

      Vladimír Mlynárik and Mary C. McKenna

      Version of Record online: 23 OCT 2013 | DOI: 10.1111/jnc.12448

      Read the full articleNon-invasive detection of neurochemical changes prior to overt pathology in a mouse model of spinocerebellar ataxia type 1’ on doi: 10.1111/jnc.12435.

  3. REVIEW

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      Molecular targets underlying SUMO-mediated neuroprotection in brain ischemia (pages 580–591)

      Vasco Silveirinha, Gary J. Stephens and Helena Cimarosti

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12347

  4. SHORT COMMUNICATIONS

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. You have free access to this content
      Presenilin 2 influences miR146 level and activity in microglia (pages 592–599)

      Suman Jayadev, Amanda Case, Betty Alajajian, Alison J. Eastman, Thomas Möller and Gwenn A. Garden

      Version of Record online: 30 SEP 2013 | DOI: 10.1111/jnc.12400

      Thumbnail image of graphical abstract

      Presenilin 2 (PS2), a membrane associated protease, has been implicated in the pathogenesis of Alzheimer disease. We have previously shown that PS2 plays an important role in curbing the proinflammatory response in microglia. Here, we report the novel finding that PS2 participates in maintaining the basal and cytokine induced expression of the innate immunity regulating microRNA, miR146. These data suggest one mechanism by which PS2 works to reign in proinflammatory microglial behavior and that PS2 dysfunction or deficiency could thus result in unchecked proinflammatory activation contributing to neurodegeneration.

  5. Short Communications

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. You have free access to this content
      Levels of plasma sulfatides C18 : 0 and C24 : 1 correlate with disease status in relapsing–remitting multiple sclerosis (pages 600–604)

      Ana L Moyano, Katarzyna Pituch, Guanan Li, Richard van Breemen, Jan E Mansson and Maria I Givogri

      Version of Record online: 9 JUL 2013 | DOI: 10.1111/jnc.12341

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      Sulfatides are glycolipids highly enriched in myelin that have been associated with multiple sclerosis (MS). In this study, we have found a positive correlation between levels of specific sulfatides in plasma and increased disability in patients with relapsing-remitting MS. These findings underline the potential use of these molecules as biomarkers for MS.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Peptidylglycine α-amidating monooxygenase heterozygosity alters brain copper handling with region specificity (pages 605–619)

      Eric D. Gaier, Megan B. Miller, Martina Ralle, Dipendra Aryal, William C. Wetsel, Richard E. Mains and Betty A. Eipper

      Version of Record online: 13 OCT 2013 | DOI: 10.1111/jnc.12438

      Thumbnail image of graphical abstract

      Atp7a, a Cu-transporting P-type ATPase, is localized to the trans-Golgi network and to vesicles distributed throughout the dendritic arbor. Tissue-specific alterations in Atp7a expression were found in mice heterozygous for peptidylglycine α-amidating monooxygenase (PAM), an essential neuropeptide-synthesizing cuproenzyme. Atp7a and PAM are highly expressed in amygdalar interneurons. Reduced amygdalar expression of Atox-1 and Atp7a in PAM heterozygous mice may lead to reduced synaptic Cu levels, contributing to the behavioral and neurochemical alterations seen in these mice.

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      Differential regulation of CaMKIIα interactions with mGluR5 and NMDA receptors by Ca2+ in neurons (pages 620–631)

      Dao-Zhong Jin, Ming-Lei Guo, Bing Xue, Li-Min Mao and John Q. Wang

      Version of Record online: 17 SEP 2013 | DOI: 10.1111/jnc.12434

      Thumbnail image of graphical abstract

      We show that activation of mGluR5 with a selective agonist triggers intracellular Ca2+ release in striatal neurons. Released Ca2+ dissociates preformed CaMKIIα from mGluR5 and meanwhile promotes active CaMKIIα to bind to the adjacent NMDAR GluN2B subunit, which enables CaMKIIα to phosphorylate GluN2B at a CaMKIIα-sensitive site. This agonist-induced cascade seems to mediate crosstalk between mGluR5 and NMDA receptors in neurons.

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      Activation of α7-containing nicotinic receptors on astrocytes triggers AMPA receptor recruitment to glutamatergic synapses (pages 632–643)

      Xulong Wang, Giordano Lippi, David M. Carlson and Darwin K. Berg

      Version of Record online: 30 SEP 2013 | DOI: 10.1111/jnc.12436

      Thumbnail image of graphical abstract

      We find that activation of nicotinic receptors on astrocytes releases a component that specifically recruits AMPA receptors to glutamatergic synapses. The recruitment appears to occur preferentially at what may be ‘silent synapses’, that is, synapses that have all the components required for glutamatergic transmission (including NMDA receptors) but lack sufficient AMPA receptors to generate a response. The results are unexpected and open up new possibilities for mechanisms underlying network formation and synaptic plasticity.

    4. Neuroinflammation & Neuroimmunology

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      Cytochrome c dysregulation induced by HIV infection of astrocytes results in bystander apoptosis of uninfected astrocytes by an IP3 and calcium-dependent mechanism (pages 644–651)

      Eliseo A. Eugenin and Joan W. Berman

      Version of Record online: 20 OCT 2013 | DOI: 10.1111/jnc.12443

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      We demonstrated that HIV infection of astrocytes protects infected cells from apoptosis but results in cell death of surrounding uninfected astrocytes by a mechanism that is dependent on gap junction channels, dysregulation of mitochondrial cytochrome C (CytC), and cell to cell diffusion of inositol trisphosphate (IP3) and calcium. Our data provide essential information about generation of brain reservoirs and the mechanism of toxicity mediated by the virus.

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      Acrolein stimulates the synthesis of IL-6 and C-reactive protein (CRP) in thrombosis model mice and cultured cells (pages 652–659)

      Ryotaro Saiki, Daisuke Hayashi, Yukiko Ikuo, Kazuhiro Nishimura, Itsuko Ishii, Kaoru Kobayashi, Kan Chiba, Toshihiko Toida, Keiko Kashiwagi and Kazuei Igarashi

      Version of Record online: 1 JUL 2013 | DOI: 10.1111/jnc.12336

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      The combined measurements of protein-conjugated acrolein (PC-Acro), IL-6, and C-reactive protein (CRP) in plasma were useful for identifying silent brain infarction. The aim of this study was to determine whether acrolein causes increased production of IL-6 and CRP, and indeed acrolein increased IL-6 synthesis and IL-6 in turn increased CRP synthesis. Furthermore, IL-6 decreased acrolein toxicity in several cell lines.

  7. HIGHLIGHTED ARTICLE

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. ORIGINAL ARTICLES

      Molecular Basis of Disease
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      Non-invasive detection of neurochemical changes prior to overt pathology in a mouse model of spinocerebellar ataxia type 1 (pages 660–668)

      Uzay E. Emir, Howard Brent Clark, Manda L. Vollmers, Lynn E. Eberly and Gülin Öz

      Version of Record online: 17 SEP 2013 | DOI: 10.1111/jnc.12435

      Thumbnail image of graphical abstract

      We measured cerebellar neurochemical alterations in a knock-in mouse model of spinocerebellar ataxia type 1, a hereditary movement disorder, using ultra-high field magnetic resonance spectroscopy (MRS). Very early neurochemical alterations were detectable prior to overt pathology in the volume-of-interest for MRS. Alterations were indicative of osmolytic changes and of disturbances in membrane phospholipid and energy metabolism.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12448.

  8. ORIGINAL ARTICLES

    1. Top of page
    2. PREFACE
    3. EDITORIAL HIGHLIGHT
    4. REVIEW
    5. SHORT COMMUNICATIONS
    6. Short Communications
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. Molecular Basis of Disease

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      Critical role of Nrf2 in oxidative stress-induced retinal ganglion cell death (pages 669–680)

      Noriko Himori, Kotaro Yamamoto, Kazuichi Maruyama, Morin Ryu, Keiko Taguchi, Masayuki Yamamoto and Toru Nakazawa

      Version of Record online: 17 JUN 2013 | DOI: 10.1111/jnc.12325

      Thumbnail image of graphical abstract

      This study suggests that NF-E2 related factor 2 (Nrf2), a transcription factor, plays a pivotal role in counteracting oxidative stress. Most importantly, a neuroprotective effect against oxidative stress-induced retinal ganglion cell (RGC) death was achieved with the pharmacological Nrf2 activator CDDO-Im. This suggests that pharmacological treatment to up-regulate Nrf2 signaling may be a new therapeutic technique to protect RGCs.

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      CSF levels of the neuronal injury biomarker visinin-like protein-1 in Alzheimer's disease and dementia with Lewy bodies (pages 681–690)

      Xinni Luo, Le Hou, Haishan Shi, Xiaomei Zhong, Yufeng Zhang, Dong Zheng, Yan Tan, Guoyan Hu, Nan Mu, Jianping Chan, Xinru Chen, Yaxiu Fang, Fengchun Wu, Hongbo He and Yuping Ning

      Version of Record online: 26 JUN 2013 | DOI: 10.1111/jnc.12331

      Thumbnail image of graphical abstract

      Neuronal Ca2+-sensor protein VILIP-1 has been implicated in the calcium-mediated neuronal injury and pathological change of AD. The CSF VILIP-1 and VILIP-1/Aβ1-42 levels had enough diagnostic accuracy to allow the detection and differential diagnosis of AD. CSF VILIP-1 is a useful biomarker for AD. Evaluating the CSF levels of VILIP-1 in AD and DLB patients could facilitate clinical diagnosis.

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      Endothelial nitric oxide deficiency promotes Alzheimer's disease pathology (pages 691–700)

      Susan A. Austin, Anantha V. Santhanam, David J. Hinton, Doo-Sup Choi and Zvonimir S. Katusic

      Version of Record online: 27 JUN 2013 | DOI: 10.1111/jnc.12334

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      Cardiovascular risk factors are associated with increased incidence of Alzheimer's disease (AD). A common feature of these risk factors is decreased endothelial nitric oxide (NO). We observed, in mice deficient in endothelial nitric oxide synthase, increased amyloid precursor protein (APP), β-site APP cleaving enzyme 1, amyloid beta levels, microglial activation, and impaired spatial memory. This suggests chronic loss of endothelial NO may be an important contributor to the pathogenesis of sporadic AD.

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      Unfolded protein response to global ischemia following 48 h of reperfusion in the rat brain: the effect of age and meloxicam (pages 701–710)

      Irene L. Llorente, Taiana C. Burgin, Diego Pérez-Rodríguez, Beatriz Martínez-Villayandre, Carlos C. Pérez-García and Arsenio Fernández-López

      Version of Record online: 4 JUL 2013 | DOI: 10.1111/jnc.12337

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      In this study, we conclude that the unfolded protein response (UPR) to ischemic/reperfusion insult is age- and probably inflammation-dependent and could play an important role in ischemic vulnerability. The UPR strongly decreased in aged rats, suggesting a reduced ability for cell survival. The increase in the mRNA levels of UPR gene transcripts in 3-month-old animals was abolished or even reverted by treatment with meloxicam, an anti-inflammatory agent.

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      The Parkinson's disease-associated gene PINK1 protects neurons from ischemic damage by decreasing mitochondrial translocation of the fission promoter Drp1 (pages 711–722)

      Yanxin Zhao, Fangzhe Chen, Shufen Chen, Xueyuan Liu, Mei Cui and Qiang Dong

      Version of Record online: 30 JUN 2013 | DOI: 10.1111/jnc.12340

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      In this study by employing an oxygen–glucose deprivation (OGD) neuronal model, we explored the function of PINK1 in cerebral ischemia. We indicated that PINK1 significantly ameliorated OGD induced cell death and energy disturbance including reduced ATP generation and collapse of mitochondrial membrane potential by attenuating mitochondrial translocation of Drp1, which maintains mitochondrial function and inhibits ischemia-induced mitochondrial fission.

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      Ischemic post-conditioning facilitates brain recovery after stroke by promoting Akt/mTOR activity in nude rats (pages 723–732)

      Rong Xie, Peng Wang, Xunming Ji and Heng Zhao

      Version of Record online: 8 JUL 2013 | DOI: 10.1111/jnc.12342

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      Post-conditioning did not attenuate infarction in nude rats measured 2 days post-stroke, but improved neurological function in nude rats and reduced brain damage 30 days after stroke. It resulted in increased-activities of Akt and mTOR, S6K and p-4EBP1. The mTOR inhibitor rapamycin abolished the long-term protective effects of IPostC.

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