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Journal of Neurochemistry

Cover image for Vol. 130 Issue 2

July 2014

Volume 130, Issue 2

Pages i–ix, 161–323

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      Issue Cover (July 2014)

      Version of Record online: 7 JUL 2014 | DOI: 10.1111/jnc.12571

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      Front cover: Poly-Ɛ-caprolactone aligned fibres, diameter 0.45µm, of a bioscaffold employed to culture astrocytes in three dimensions. J. Neurochem. 2014, vol. 130 (2), pp. 215–226.

      Read the full article on doi: 10.1111/jnc.12702

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      Issue Information (pages i–ii)

      Version of Record online: 7 JUL 2014 | DOI: 10.1111/jnc.12572

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      In this Issue (pages iii–ix)

      Version of Record online: 7 JUL 2014 | DOI: 10.1111/jnc.12573

  4. EDITORIAL HIGHLIGHT

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      Targeting calpain-mediated proteolysis and peptide signaling as a strategy to reduce injury in multiple sclerosis (pages 161–164)

      Thad A. Rosenberger

      Version of Record online: 21 MAY 2014 | DOI: 10.1111/jnc.12732

      Read the full article ‘Effects of a novel orally administered calpain inhibitor SNJ-1945 on immunomodulation and neurodegeneration in a murine model of multiple sclerosis’ on page 268

  5. REVIEW ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
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      Macrophages and CNS remyelination (pages 165–171)

      Veronique E. Miron and Robin J. M. Franklin

      Version of Record online: 26 MAR 2014 | DOI: 10.1111/jnc.12705

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      Here, we review the roles of microglia, monocytes and the macrophages, which they give rise to in creating lesion environments favourable to remyelination, highlighting the specific roles of activation phenotypes and how the pro-regenerative role of the innate immune system is altered by ageing.

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      mTOR complex 1: a key player in neuroadaptations induced by drugs of abuse (pages 172–184)

      Jeremie Neasta, Segev Barak, Sami Ben Hamida and Dorit Ron

      Version of Record online: 19 APR 2014 | DOI: 10.1111/jnc.12725

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      Recent studies suggesting that exposure to diverse classes of drugs of abuse as well as exposure to drug-associated memories lead to mTORC1 kinase activation in the limbic system. In turn, mTORC1 controls the onset and the maintenance of pathological neuroadaptions that underlie several features of drug addiction such as drug seeking and relapse. Therefore, we propose that targeting mTORC1 and its effectors is a promising strategy to treat drug disorders.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      α6β2*-subtype nicotinic acetylcholine receptors are more sensitive than α4β2*-subtype receptors to regulation by chronic nicotine administration (pages 185–198)

      Michael J. Marks, Sharon R. Grady, Outi Salminen, Miranda A. Paley, Charles R. Wageman, J. Michael McIntosh and Paul Whiteaker

      Version of Record online: 19 APR 2014 | DOI: 10.1111/jnc.12721

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      This study examined dose–response relationships for murine α6β2*-nicotinic acetylcholine receptor (nAChR) down-regulation by chronic nicotine treatment. The ID50 value for α6β2* down-regulation (35 nM) is ≈ 3x lower than the ED50 value for α4β2* nAChR up-regulation (95 nM), both well within the range reached by human smokers. Chronic nicotine treatment altered α6β2*- and α4β2*-nAChR-mediated [3H]-dopamine release from striatal and olfactory tubercle synaptosomes, but dopaminergic parameters were largely unaffected. We conclude that functional changes are primarily driven by altered nAChR activity.

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      Identification and quantification of neuropeptides in naïve mouse spinal cord using mass spectrometry reveals [des-Ser1]-cerebellin as a novel modulator of nociception (pages 199–214)

      Jie Su, Katalin Sandor, Karl Sköld, Tomas Hökfelt, Camilla I. Svensson and Kim Kultima

      Version of Record online: 6 MAY 2014 | DOI: 10.1111/jnc.12730

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      Neuropeptides involved in nociceptive processes are more likely to be expressed in the dorsal than the ventral horn of spinal cord. Well-characterized full-length neuropeptides as well as uncharacterized neuropeptides were quantified by mass spectrometry. The CBLN1-derived peptide [des-Ser1]-cerebellin (desCER) is predominantly expressed in the dorsal horn, and intrathecal injection of desCER induced a dose-dependent mechanical hypersensitivity.

    3. Brain Development & Cell Differentiation

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      3D Electrospun scaffolds promote a cytotrophic phenotype of cultured primary astrocytes (pages 215–226)

      Chew L. Lau, Michelle Kovacevic, Tine S. Tingleff, John S. Forsythe, Holly S. Cate, Daniel Merlo, Cecilia Cederfur, Francesca L. Maclean, Clare L. Parish, Malcolm K. Horne, David R. Nisbet and Philip M. Beart

      Version of Record online: 9 APR 2014 | DOI: 10.1111/jnc.12702

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      Astrocytes exist in phenotypes with pro-survival and destructive components, and their biology can be modulated by changing phenotype. Our findings demonstrate murine astrocytes adopt a healthy phenotype when cultured in 3D. Astrocytes proliferate and extend into poly-ε-caprolactone scaffolds displaying 3D stellated morphologies with reduced GFAP expression and actin stress fibres, plus a cytotrophic gene profile. Bioengineered 3D scaffolds have potential to direct inflammation to aid regenerative neurobiology.

      Cover Image for this issue: doi: 10.1111/jnc.12571.

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      Cyr61 activates retinal cells and prolongs photoreceptor survival in rd1 mouse model of retinitis pigmentosa (pages 227–240)

      Joanna Kucharska, Patricia del Río, Blanca Arango-Gonzalez, Matteo Gorza, Annette Feuchtinger, Stefanie M. Hauck and Marius Ueffing

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12704

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      We propose the following model of Cyr61 neuroprotection within the retina: Cyr61 stimulates retinal Müller glial (RMG) and retinal pigment epithelium (RPE) cells and activates PI3K/Akt, mitogen-activated protein kinase(MAPK)/Erk and Janus kinase(JAK)/Stat-signalling pathways in these cells. Phosphorylated Stat3 and Erk1/2 presumably translocate to the nucleus, induce transcriptional changes, which increase secretion of neuroprotective agents that protect photoreceptors (PR) from mutation-induced death.

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      Cortical-layer-specific effects of PACAP and tPA on interneuron migration during post-natal development of the cerebellum (pages 241–254)

      Emilie Raoult, Magalie Bénard, Hitoshi Komuro, Alexis Lebon, Denis Vivien, Alain Fournier, Hubert Vaudry, David Vaudry and Ludovic Galas

      Version of Record online: 19 APR 2014 | DOI: 10.1111/jnc.12714

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      Crucial role of tissue plasminogen activator (tPA) in interneuron migration. Interneuron migration is a critical step for normal establishment of neuronal network. This study indicates that, in the post-natal cerebellum, tPA facilitates the opposite migration of immature excitatory granule neurons (GN) and immature inhibitory basket/stellate cells (B/SC) along the same migratory route. These data show that tPA exerts a pivotal role in neurodevelopment.

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      PI3K-p110-alpha-subtype signalling mediates survival, proliferation and neurogenesis of cortical progenitor cells via activation of mTORC2 (pages 255–267)

      Shalaka Dhanraj Wahane, Nicole Hellbach, Mirja Tamara Prentzell, Stefan Christopher Weise, Riccardo Vezzali, Clemens Kreutz, Jens Timmer, Kerstin Krieglstein, Kathrin Thedieck and Tanja Vogel

      Version of Record online: 3 MAY 2014 | DOI: 10.1111/jnc.12718

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      Within developing cortical cells TGFβ- and IGF-signalling activities are timely separated. TGFβ dominates in E16.5-derived cells and drives neuronal differentiation. IGF influences survival, proliferation and neuronal differentiation in E13.5-derived cells. mTORC2-signalling in E16.5-derived cells influences survival, proliferation and differentiation, activated through PI3K-p110-alpha. PI3K-p110-beta-signalling activates a different mTORC2. Both PI3K/mTORC2-signalling pathways are required but not directly activated in TGFβ-mediated neuronal differentiation.

  7. HIGHLIGHTED ARTICLE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. ORIGINAL ARTICLES

      Neuroinflammation & Neuroimmunology
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      Effects of a novel orally administered calpain inhibitor SNJ-1945 on immunomodulation and neurodegeneration in a murine model of multiple sclerosis (pages 268–279)

      Nicole Trager, Amena Smith, Gerald Wallace IV, Mitsuyoshi Azuma, Jun Inoue, Craig Beeson, Azizul Haque and Naren L. Banik

      Version of Record online: 12 FEB 2014 | DOI: 10.1111/jnc.12659

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      Multiple sclerosis (MS) pathology is marked by inflammation and infiltration of myelin-specific T cells into the central nervous system. Inflammation leads to neurodegeneration in progressive MS which also leads to epitope spreading, feedback looping to more inflammation. Calpain can play a role in both arms of the disease. Here, oral dosing with SNJ-1945, a novel water-soluble calpain inhibitor, reduces experimental autoimmune encephalomyelitis clinical scores in vivo and has a two-pronged effect via anti-inflammation and protection against neurodegeneration.

      Read the Editorial Highlight for this article on page 161.

  8. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. HIGHLIGHTED ARTICLE
    9. ORIGINAL ARTICLES
    1. Neuroinflammation & Neuroimmunology

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      SNJ-1945, a calpain inhibitor, protects SH-SY5Y cells against MPP+ and rotenone (pages 280–290)

      Varduhi H. Knaryan, Supriti Samantaray, Sookyoung Park, Mitsuyoshi Azuma, Jun Inoue and Naren L. Banik

      Version of Record online: 16 DEC 2013 | DOI: 10.1111/jnc.12629

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      SH-SY5Y cells, differentiated as dopaminergic (TH positive) and cholinergic (ChAT positive), were used as in vitro models for Parkinson's disease. MPP+ and rotenone induced up-regulation of calpain, expression, and activity as a common mechanism of neurodegeneration. SNJ-1945, a novel calpain inhibitor, protected both the cell phenotypes against MPP+ and rotenone.

    2. Molecular Basis of Disease

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      A mutation protective against Alzheimer's disease renders amyloid β precursor protein incapable of mediating neurotoxicity (pages 291–300)

      Yuichi Hashimoto and Masaaki Matsuoka

      Version of Record online: 9 APR 2014 | DOI: 10.1111/jnc.12717

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      The A598T mutation of amyloid precursor protein APP is linked to a reduction in the incidence rate of Alzheimer's disease (AD). This study shows that TGFβ2 causes death in neuronal cells expressing wild-type APP, but not in those expressing the AD-protective mutant of APP, suggesting that the AD-protective mutation of APP reduces the incidence rate of AD by attenuating the APP-mediated intracellular death signal.

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      Brain proteomics identifies potential simvastatin targets in acute phase of stroke in a rat embolic model (pages 301–312)

      Mireia Campos-Martorell, Nelida Salvador, Marta Monge, Francesc Canals, Lidia García-Bonilla, Mar Hernández-Guillamon, María Irene Ayuso, Pilar Chacón, Anna Rosell, Alberto Alcazar and Joan Montaner

      Version of Record online: 30 APR 2014 | DOI: 10.1111/jnc.12719

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      Our aim was to study statins benefits when administered during the acute phase of stroke and to explore its mechanisms of action through brain proteomics assay. Using an embolic model, simvastatin-treated rats showed significant infarct volume reduction and neurological improvement compared to vehicle-treated group. Analyzing their homogenated brains by two-dimensional fluorescence Difference in Gel Electrophoresis (DIGE) technology, we concluded that the protective effect of simvastatin can be attributable to oxidative stress response attenuation and blood–brain barrier protection after cerebral ischemia.

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      Evidence for an angiotensin-(1-7) neuropeptidase expressed in the brain medulla and CSF of sheep (pages 313–323)

      Allyson C. Marshall, Nancy T. Pirro, James C. Rose, Debra I. Diz and Mark C. Chappell

      Version of Record online: 19 APR 2014 | DOI: 10.1111/jnc.12720

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      Angiotensin-(1-7) actions are mediated by the AT7/Mas receptor and include reduced blood pressure, decreased oxidative stress, enhanced baroreflex sensitivity, and increased nitric oxide (NO). Ang-(1-7) is directly formed from Ang I by neprilysin (NEP). We identify a new pathway for Ang-(1-7) metabolism in the brain distinct from angiotensin-converting enzyme-dependent hydrolysis. The Ang-(1-7) endopeptidase (A7-EP) degrades the peptide to Ang-(1-4) and may influence central Ang-(1-7) tone.

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