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Journal of Neurochemistry

Cover image for Vol. 120 Issue 5

March 2012

Volume 120, Issue 5

Pages 641–850

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. ERRATUM
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      Seeding plaques in Alzheimer’s disease (pages 641–643)

      Marco A. M. Prado and Gerald Baron

      Article first published online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07574.x

  2. REVIEW ARTICLE

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. ERRATUM
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      The S100B protein in biological fluids: more than a lifelong biomarker of brain distress (pages 644–659)

      Fabrizio Michetti, Valentina Corvino, Maria Concetta Geloso, Wanda Lattanzi, Camilla Bernardini, Laura Serpero and Diego Gazzolo

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07612.x

  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. ERRATUM
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      Exogenous seeding of cerebral β-amyloid deposition in βAPP-transgenic rats (pages 660–666)

      Rebecca F. Rosen, Jason J. Fritz, Jeromy Dooyema, Amarallys F. Cintron, Tsuyoshi Hamaguchi, James J. Lah, Harry LeVine III, Mathias Jucker and Lary C. Walker

      Article first published online: 18 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07551.x

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      Jump-starting amyloid in resistant brains. Cerebral amyloid-β (Aβ) deposition can be seeded in the brains of susceptible animals by brain extracts containing aggregated Aβ, but whether Aβ aggregation can be seeded in resistant models is uncertain. Using Alzheimer brain extracts, we induced Aβ deposition in the hippocampal formation of Aβ-precursor protein-transgenic rats that do not normally generate senile plaques. Our findings highlight the role of corruptive protein templating in the initiation of Aβ amyloidosis, and show that this process can be actuated even in a relatively resistant animal model.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. ERRATUM
    1. Brain Development & Cell Differentiation

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      Control of neurite outgrowth by RhoA inactivation (pages 684–698)

      Chan-Young Jeon, Mi-Young Moon, Jong-Hyun Kim, Hee-Jun Kim, Jae-Gyu Kim, Yi Li, Jae-Kwang Jin, Pyeung-Hyeun Kim, Hyoung-Chun Kim, Kathryn E. Meier, Yong-Sun Kim and Jae-Bong Park

      Article first published online: 24 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07564.x

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      RhoA inactivation is required for neurite outgrowth of PC12 cells in response to cAMP. Hereby, we elucidated the mechanism of RhoA inactivation by cAMP: the phosphorylation of RhoA and the activation of p190RhoGAP and Rap1/ARAP3 participate in RhoA inactivation. Because neuronal regeneration is induced by RhoA inactivation, Rho inhibitors are emerging as the therapeutic reagents to promote neuronal regeneration.

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      Dual REST-dependence of L1CAM: from gene expression to alternative splicing governed by Nova2 in neural cells (pages 699–709)

      Joanna Mikulak, Sara Negrini, Andrijana Klajn, Rosalba D’Alessandro, Domenico Mavilio and Jacopo Meldolesi

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07626.x

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      Neural mRNA splicing, a new function of REST. Differential mRNA splicing is a key mechanism of brain specificity. Here, we show that REST, the master factor of neural cells, controls the transcription of the Nova2 gene and thus the splicing, whether neural and highly effective or non-neural, of the adhesion protein L1CAM. Most likely the same mechanism operates on many other spliced products specific of the brain.

    4. Neuroinflammation & Neuroimmunology

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      STAT3 signaling after traumatic brain injury (pages 710–720)

      Anthony A. Oliva, Yuan Kang, Juliana Sanchez-Molano, Concepción Furones and Coleen M. Atkins

      Article first published online: 31 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07610.x

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      Is STAT3 activation during traumatic brain injury pro- or anti-inflammatory? STAT3 activation can either worsen or improve recovery after spinal cord injury or ischemia, depending upon the cell type and signaling pathways involved. Here, we used fluid-percussion brain injury, a clinically relevant model of traumatic brain injury, and found that STAT3 was rapidly activated and translocated to nuclei within astrocytes. This resulted in a stimulation of both pro- and anti-inflammatory gene expression.

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      Nogo-66 inhibits adhesion and migration of microglia via GTPase Rho pathway in vitro (pages 721–731)

      Jun Yan, Xiao Zhou, Jing-Jing Guo, Lei Mao, Yi-Jin Wang, Jing Sun, Li-Xin Sun, Lu-Yong Zhang, Xin-Fu Zhou and Hong Liao

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07619.x

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      This article explores the role of NgR expressed on microglia in the regulation of microglia behavior. Results demonstrated that Nogo-66 triggered microglia anti-adhesion and inhibited their migration in vitro, which was mediated by NgR and its downstream signal transducers RhoA and Cdc42. The finding revealed the Nogo-66/NgR pathway may modulate neuroinflammation via mediating microglia adhesion and migration, and blocking NgR may be beneficial to promote microglia migrating out injury site. This may help targeting NgR for treating central nervous system diseases related with inflammation.

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      Autoreactive-Aβ antibodies promote APP β-secretase processing (pages 732–740)

      Juan Deng, Huayan Hou, Brian Giunta, Takashi Mori, Yan-Jiang Wang, Frank Fernandez, Sascha Weggen, Wataru Araki, Demian Obregon and Jun Tan

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07629.x

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      Autoreactive Aβ may be deleteriousAlthough many studies have focused on the relative concentrations or binding affinities of autoantibodies against Aβ-related proteins in AD and aging, data regarding their functional properties are limited. We show that naturally occurring Aβ-reactive autoantibodies isolated from AD patients, but not from healthy age-matched controls, promote amyloidogenic APP processing. Such results suggest a novel etiology for sporadic AD because antibodies binding to N-terminal Aβ regions, such as (a) Aβ17-26 or (b) Aβ1-17, also bind extracellular corresponding regions of the parent (APP) molecule and demonstrate a functional capacity to alter APP processing in a manner promoting Aβ generation.

    7. Neuronal Plasticity & Behavior

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      Ectodomain shedding of nectin-1 regulates the maintenance of dendritic spine density (pages 741–751)

      Seung T. Lim, Allison Chang, Rita E. Giuliano and Howard J. Federoff

      Article first published online: 16 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07592.x

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      Ectodomain shedding of nectin-1 regulates the maintenance of dendritic spine density What is the role of secretase-mediated ectodomain shedding of synaptic cell adhesion molecules in synaptogenesis? The expression of shedding refractory nectin-1 mutants dramatically increased the density of dendritic spines. Our data suggest that ectodomain shedding of synaptic adhesion molecules by sheddases is a regulator of synaptic plasticity through its modulation of synaptic connections.

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      A novel anti-inflammatory role for spleen-derived interleukin-10 in obesity-induced hypothalamic inflammation (pages 752–764)

      Koro Gotoh, Megumi Inoue, Takayuki Masaki, Seiichi Chiba, Takanobu Shimasaki, Hisae Ando, Kansuke Fujiwara, Isao Katsuragi, Tetsuya Kakuma, Masataka Seike, Toshiie Sakata and Hironobu Yoshimatsu

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07617.x

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      Obesity may be associated with a systemic low-grade inflammation that affects obesity-related metabolic disorders. Splenectomy (SPX)-induced inflammatory changes in the hypothalamus were inhibited by the systemic administration of IL-10 and SPX had no effect on hypothalamic inflammatory responses in the IL-10-deficient mice. Thus, spleen-derived IL-10 may be a key to treat the pathogenesis of obesity including hypothalamic inflammation.

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      Pre-synaptic dopamine D3 receptor mediates cocaine-induced structural plasticity in mesencephalic dopaminergic neurons via ERK and Akt pathways (pages 765–778)

      Ginetta Collo, Federica Bono, Laura Cavalleri, Laura Plebani, Emilio Merlo Pich, Mark J. Millan, Pier Franco Spano and Cristina Missale

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07618.x

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      Psychostimulants promote structural plasticity in neurons of the terminal fields of the mesocorticolimbic dopaminergic system, but it is unclear if morphological reorganization occurs also in the neurons that originate these projections. When primary cultures of mesencephalic dopaminergic neurons from the mouse embryos were exposed to cocaine, a dopamine D3 autoreceptor (D3R)-dependent activation of ERK and PI3K-Akt pathways occurred, leading to a later expansion of dendrite arborization and soma size. In utero exposure to cocaine also increased the soma area of dopaminergic neurons, but only in newborns of wild-type mice, not in D3KO. Our results indicate that D3R is a necessary mediator of the cocaine-dependent structural remodeling of dopaminergic neurons via ERK and PI3K-Akt activation, suggesting a possible mechanism of action for the anti-addictive behavioral effects of D3 antagonists.

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      Activation of mu opioid receptors in the striatum differentially augments methamphetamine-induced gene expression and enhances stereotypic behavior (pages 779–794)

      Kristen A. Horner, John C. Hebbard, Anna S. Logan, Golda A. Vanchipurakel and Yamiece E. Gilbert

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07620.x

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      Think twice before mixing your psychostimulants with opiates. Mu opioid receptors are densely expressed in the striatum, a major target nucleus for the actions of methamphetamine. We examined whether activation of these receptors would alter methamphetamine-induced behaviour and gene expression. Mu opioid receptor activation intensified methamphetamine-induced stereotypy and gene expression in the striatum, indicating that the mu opioid system can enhance the behavioural and genomic responses to methamphetamine.

    11. Molecular Basis of Disease

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      Improvement of cognitive function in Alzheimer’s disease model mice by genetic and pharmacological inhibition of the EP4 receptor (pages 795–805)

      Tatsuya Hoshino, Takushi Namba, Masaya Takehara, Naoya Murao, Takahide Matsushima, Yukihiko Sugimoto, Shuh Narumiya, Toshiharu Suzuki and Tohru Mizushima

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07567.x

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      The purpose of this study is to know the role of EP2 and EP4 receptors in cognitive performance in APP23 mice, model mice for Alzheimer’s disease. Results suggest that inhibition of the EP4 receptor improves the cognitive function of APP23 mice and that EP4 receptor antagonists, such as AE3-208, are therapeutically beneficial for the prevention and treatment of AD.

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      Serotonergic modulation of receptor occupancy in rats treated with l-DOPA after unilateral 6-OHDA lesioning (pages 806–817)

      Adjmal Nahimi, Mette Høltzermann, Anne M. Landau, Mette Simonsen, Steen Jakobsen, Aage Kristian Olsen Alstrup, Kim Vang, Arne Møller, Gregers Wegener, Albert Gjedde and Doris J. Doudet

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07598.x

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      l-DOPA induced dopamine release from serotonergic neurons activate dopamine D2 receptors in Parkinson’s disease The effect of a 5-HT1A agonist on the l-DOPA induced decrease in [11C]raclopride binding was evaluated in an unilateral lesioned animal model of Parkinson’s disease (PD). The baseline increase of [11C]raclopride binding in lesioned striatum was eliminated by the l-DOPA challenge, while the concurrent administration of 8-OHDPAT prevented this. This study concludes that evaluating the effect(s) of pharmacological challenges by one or multiple drugs may be a feasible goal in human subjects with PD.

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      Vascular endothelial growth factor in the ischemic retina and its regulation by somatostatin (pages 818–829)

      Davide Cervia, Elisabetta Catalani, Massimo Dal Monte and Giovanni Casini

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07622.x

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      In retinal disease, ischemia causes cell death. We investigated whether ischemia may also initiate pathological angiogenesis mediated by vascular endothelial growth factor (VEGF). This study identified a rapid VEGF response to ischemia, in which VEGF is released by damaged neurons and is taken up by endothelial cells of retinal capillaries. Activation of somatostatin subtype 2 receptor (sst2) is known to reduce cell death. Similarly, we found that the VEGF response is also limited by sst2.

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      Identification of differentially expressed microRNAs and their PKC-isoform specific gene network prediction during hypoxic pre-conditioning and focal cerebral ischemia of mice (pages 830–841)

      Cuiying Liu, Zhifeng Peng, Nan Zhang, Li Yu, Song Han, Dongguo Li and Junfa Li

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07624.x

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      Differentially expressed miRNAs in cerebral cortex of mice following hypoxic pre-conditioning (HPC) and middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia Differentially expressed miRNAs were identified in cerebral cortex of mice following HPC and MCAO. The miRNA-gene-network of these 19 specified miRNAs target genes of cPKCβII, γ and nPKCε-interacting proteins involved in HPC-induced neuroprotection was predicted using bioinformatics analyses of genome databases. Furthermore, the down-regulated miR-615-3p during HPC had a detrimental effect on the oxygen-glucose deprivation (OGD)-induced N2A cell injury.

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      Alteration of endocannabinoid system in human gliomas (pages 842–849)

      Xiyue Wu, Lijun Han, Xiaolin Zhang, Long Li, Changzhen Jiang, Yan Qiu, Rui Huang, Baoying Xie, ZhiXiong Lin, Jie Ren and Jin Fu

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07625.x

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      Endocannabinoids are neuromodulatory lipids mediating anti-proliferation, anti-angiogenesis and pro-apoptosis processes. To understand the role of endocannabinoid system in tumorigenesis, we demonstrated that endocananbinoid signals, CB1 and CB2, were elevated in human gliomas. We concluded that the changes of anandamide and 2-AG contents in different stages of gliomas might serve as the potential biomarkers for glial tumor malignancy.

  5. ERRATUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. ERRATUM
    1. You have free access to this content
      Erratum (page 850)

      Article first published online: 4 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07627.x

      This article corrects:

      Reactive Oxygen Species and the Central Nervous System

      Vol. 59, Issue 5, 1609–1623, Article first published online: 5 OCT 2006

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