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Journal of Neurochemistry

Cover image for Vol. 123 Issue 1

October 2012

Volume 123, Issue 1

Pages 1–202

  1. REVIEW

    1. Top of page
    2. REVIEW
    3. SHORT COMMUNICATIONS
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. CORRIGENDUM
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  2. SHORT COMMUNICATIONS

    1. Top of page
    2. REVIEW
    3. SHORT COMMUNICATIONS
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. CORRIGENDUM
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      Quetiapine prevents oligodendrocyte and myelin loss and promotes maturation of oligodendrocyte progenitors in the hippocampus of global cerebral ischemia mice (pages 14–20)

      Xiaoying Bi, Yanbo Zhang, Bin Yan, Shaokuan Fang, Jue He, Dai Zhang, Zhijun Zhang, Jiming Kong, Qingrong Tan and Xin-Min Li

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07883.x

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      Quetiapine prevents oligodendrocyte and myelin losses and promotes oligodendrocyte maturation in the hippocampus of global cerebral ischemia mice The anti-psychotic quetiapine is used as an augment in vascular depression treatment with unknown mechanisms. This study demonstrated that quetiapine pre-treatment reduced hippocampal myelin breakdown and oligodendrocyte losses in a mouse model of vascular depression, and enhanced oligodendrocyte maturation in recovery. The results suggest the new feature of quetiapine that may be an important contributor in treating vascular depression.

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      Age-related modulation of γ-secretase activity in non-human primate brains (pages 21–28)

      Masaki Nishimura, Shin-ichiro Nakamura, Nobuyuki Kimura, Lei Liu, Toshiharu Suzuki and Ikuo Tooyama

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07884.x

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      Age-dependent modulation of γ-secretase activity may cause sporadic AD Aging is recognized as a non-genetic risk factor for Alzheimer’s disease (AD), although the underlying molecular mechanisms remain unresolved. By investigating non-human primate brains, we show that γ-secretase activity is modulated in an age-dependent manner to increase the production ratio of pathogenic Aβ42 to non- or less-pathogenic Aβ40 and that this modulation is significantly associated with Aβ accumulation. γ-Secretase activity undergoes age-related, non-genetic modulation, which may predispose aged human brains to sporadic AD

  3. ORIGINAL ARTICLES

    1. Top of page
    2. REVIEW
    3. SHORT COMMUNICATIONS
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. CORRIGENDUM
    1. Gene regulation & Genetics

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      Subcellular localization and transcription regulatory potency of KCNIP/Calsenilin/DREAM/KChIP proteins in cultured primary cortical neurons do not provide support for their role in CRE-dependent gene expression (pages 29–43)

      Priit Pruunsild and Tõnis Timmusk

      Article first published online: 27 JUN 2012 | DOI: 10.1111/j.1471-4159.2012.07796.x

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      KCNIP3/KChIP3 (voltage-dependent K+ channel interacting protein 3), alias Calsenilin and DREAM (downstream regulatory element antagonist modulator), is a multifunctional protein that modulates A-type potassium channels, affects processing of amyloid precursor protein and regulates transcription. This study was performed in order to assess the potential of KCNIP/Calsenilin/DREAM/KChIP family proteins to fulfill their functions in different cell compartments. We found that different KCNIP isoforms have distinct subcellular localization in neuronal cells and although some of the KCNIP protein isoforms are localized to the nuclei when over-expressed, they do not participate in CRE-dependent gene expression regulation and are not modulating the transcriptional activity of CREB family proteins in cultured cortical neurons.

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      NeuroD1 is required for survival of photoreceptors but not pinealocytes: Results from targeted gene deletion studies (pages 44–59)

      Margaret J. Ochocinska, Estela M. Muñoz, Shobi Veleri, Joan L. Weller, Steven L. Coon, Nikita Pozdeyev, P. Michael Iuvone, Sandra Goebbels, Takahisa Furukawa and David C. Klein

      Article first published online: 16 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07870.x

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      ‘New light on NeuroD1 and vision’1) This study was performed to investigate the post-natal role of the developmental transcription factor NeuroD1 in the retina and pineal gland. 2) The most relevant novel finding in our article is the identification of retinal and pineal transcripts that are affected by the NeuroD1 deletion and that NeuroD1 is required for proper post-natal survival and physiological function of the retinal photoreceptors. 3) This finding is important as it demonstrates the persistent role of developmental regulators throughout post-natal life and identifies new downstream targets of NeuroD1 that are important for photoreceptor homeostasis in the vertebrate retina.

    3. Signal Transduction & Synaptic Transmission

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      Calcyon, a mammalian specific NEEP21 family member, interacts with adaptor protein complex 3 (AP-3) and regulates targeting of AP-3 cargoes (pages 60–72)

      Nagendran Muthusamy, Victor Faundez and Clare Bergson

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07814.x

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      Calcyon regulates targeting of AP-3 cargoes Calcyon, a neural enriched mammalian specific protein implicated in clathrin-mediated endocytosis, contains canonical tyrosine type motifs for binding adaptor protein (AP) μ subunits. We found that targeted deletion of the calcyon gene in mice impacts the subcellular distribution of AP-3 and the localization of AP-3 cargoes. Thus, by directly interacting with AP μ subunits, calcyon regulates targeting of AP-3 cargoes in brain.

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      Type I and II positive allosteric modulators differentially modulate agonist-induced up-regulation of α7 nicotinic acetylcholine receptors (pages 73–83)

      Morten S. Thomsen and Jens D. Mikkelsen

      Article first published online: 16 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07876.x

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      It is difficult to distinguish between the actions of type I and II positive allosteric modulators (PAMs) in vivo. Here, we show that only type II PAMs inhibit agonist-induced up-regulation of α7 nicotinic receptors in vivo. As up-regulation may be an important physiological response to receptor activation, this exacts caution in the development of type II PAMs.

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      Protein phosphatase-1M and Rho-kinase affect exocytosis from cortical synaptosomes and influence neurotransmission at a glutamatergic giant synapse of the rat auditory system (pages 84–99)

      Beáta Lontay, Balázs Pál, Zoltán Serfőző, Áron Kőszeghy, Géza Szücs, Zoltán Rusznák and Ferenc Erdődi

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07882.x

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      Protein phosphatase-1M (PP1M) and RhoA-activated kinase (ROK) are present pre- and post-synaptically in both cortical synaptosomes and in a glutamatergic giant synapse of the rat auditory system. PP1 inhibition by tautomycetin (TMC) suppresses, whereas ROK inhibition by Y27632 increases neurotransmitter release. We suggest that both PP1M and ROK influence synaptic transmission by changing the phosphorylation status of several pre- and post-synaptic proteins.

    6. Neuroinflammation & Neuroimmunology

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      Genetic inactivation of the adenosine A2A receptor exacerbates brain damage in mice with experimental autoimmune encephalomyelitis (pages 100–112)

      Shu-Qin Yao, Zheng-Zheng Li, Qing-Yuan Huang, Fang Li, Zhao-Wei Wang, Elisabete Augusto, Jin-Cai He, Xiao-Tong Wang, Jiang-Fan Chen and Rong-Yuan Zheng

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07807.x

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      The role of the adenosine A2A receptor (A2AR) in development of multiple sclerosis pathology was critically evaluated in EAE model using the A2AR knockout mice. A2AR knockout exacerbates EAE-induced demyelination, axonal injury, neurobehavioral deficits, and inflammatory responses. The A2AR represents an important neuroprotective mechanism and therapeutic target to modify multiple sclerosis pathology.

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      Modulation of interferon-γ-induced glial cell activation by transforming growth factor β1: A role for STAT1 and MAPK pathways (pages 113–123)

      Rodrigo Herrera-Molina, Betsi Flores, Juan A. Orellana and Rommy von Bernhardi

      Article first published online: 22 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07887.x

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      TGFβ1 modulates glial cell inflammatory activationGlial cells activation profile determines neuronal functional outcome and survival. TGFβ1 participates in the modulation of glia-mediated cytotoxicity and radicals production. We found that TGFβ1 and IFNγ show reciprocal regulation of MAPKs and STAT1, modulating IFNγ-induced superoxide and NO production by glial cells. MAPK phosphatase MKP1 was critical for the inhibitory effect of TGFβ1. We identified a potential therapeutic target to modulate glial activation in neurodegenerative diseases

    8. Neuronal Plasticity & Behavior

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      A mutation in CLOCK leads to altered dopamine receptor function (pages 124–134)

      Sade Spencer, Melissa I. Torres-Altoro, Edgardo Falcon, Rachel Arey, Marian Marvin, Matthew Goldberg, James A. Bibb and Colleen A. McClung

      Article first published online: 27 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07857.x

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      Manic-like behavior may be because of altered dopaminergic transmission Why was this study performed? We wanted to gain a better understanding of the molecular and cellular changes that underlie bipolar disorder using a mouse model of mania (Clock mutant mice). What was the most relevant novel finding? Manic-like behavior in the Clock mutant mice is associated with increased dopamine and a shift in dopamine receptor function. Why is this finding important? If we can understand the molecular changes that lead to bipolar disorder then we can develop more targeted treatments for this disease in the future. In sum: Mice with a mutation that leads to manic-like behavior have abnormal dopamine signaling because of altered dopamine release and turnover, as well as altered dopamine receptor function. These changes in dopaminergic transmission likely underlie key components of their abnormal behavior. Future studies can use this knowledge to target this system for the development of novel therapies for bipolar disorder.

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      Transmembrane semaphorin5B is proteolytically processed into a repulsive neural guidance cue (pages 135–146)

      Kristen Browne, Wenyan Wang, Rachel Q. Liu, Matthew Piva and Timothy P. O’Connor

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07885.x

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      Neural growth cones respond to a number of directional guidance cues, including both transmembrane and secreted Semaphorin proteins. We describe the first evidence that transmembrane Semaphorin5B is proteolytically processed by metalloproteases to release a repulsive neural guidance cue. This work presents a novel mechanism whereby transmembrane Semaphorins may extend their repulsive range via modulation of local metalloprotease expression and activity.

    10. Molecular Basis of Disease

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      Calpain-cleaved type 1 inositol 1,4,5-trisphosphate receptor impairs ER Ca2+ buffering and causes neurodegeneration in primary cortical neurons (pages 147–158)

      Catherine M. Kopil, Adam P. Siebert, J. Kevin Foskett and Robert W. Neumar

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07859.x

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      Neuropathologic role of InsP 3 R1 proteolysis Calpain cleavage of InsP3R1 generates a dysregulated intracellular Ca2+ release channel however, the effects of proteolyzed InsP3R1 in neurons remain unclear. We show that expression of calpain-cleaved InsP3R1 decreases neuronal viability, alters intracellular Ca2+ homeostasis, and increases sensitivity to excitotoxic injury. These results provide insight into a possible feed-forward pathway linking disruption of Ca2+ homeostasis to neuronal death.

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      Srp20 regulates TrkB pre-mRNA splicing to generate TrkB-Shc transcripts with implications for Alzheimer’s disease (pages 159–171)

      Jenny Wong, Brett Garner, Glenda M. Halliday and John B. J. Kwok

      Article first published online: 16 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07873.x

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      The TrkB alternative transcript, TrkB-Shc, is increased in the AD hippocampus. We found that the splicing factor, Srp20, can influence TrkB pre-mRNA splicing to increase TrkB-Shc transcript levels. In the AD hippocampus, Srp20 expression is increased. Dysregulation of factors regulating TrkB pre-mRNA splicing may contribute to gene expression changes that occur in AD, thereby promoting BDNF/TrkB-TK+ signaling dysfunction and neurodegeneration.

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      Protection of dopaminergic cells by urate requires its accumulation in astrocytes (pages 172–181)

      Sara Cipriani, Cody A. Desjardins, Thomas C. Burdett, Yuehang Xu, Kui Xu and Michael A. Schwarzschild

      Article first published online: 22 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07820.x

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      Astroglial urate protects dopaminergic cells. Urate is a potent antioxidant and an inverse risk factor for Parkinson’s disease (PD). We showed that urate protects dopaminergic cells against oxidative stress in vitro. This protection depends on urate accumulation in astrocytes where it appears to trigger protective factor release. The findings suggest astrocytic urate elevation as a candidate neuroprotective strategy and novel pharmacological target for PD.

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      Neuroprotective effects of phenolic antioxidant tBHQ associate with inhibition of FoxO3a nuclear translocation and activity (pages 182–191)

      Parmvir K. Bahia, Victoria Pugh, Kimberley Hoyland, Victoria Hensley, Marcus Rattray and Robert J. Williams

      Article first published online: 16 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07877.x

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      Neuroprotective potential of the dietary phenolic antioxidant tBHQ through inhibition of FoxO3aWe wished to test whether phenolic antioxidants such as the FDA-approved food preservative tBHQ could oppose activation of FoxO3a-induced death responses in cortical and motor neurones. tBHQ inhibited NMDA-induced nuclear translocation of FoxO3a, prevented NMDA-induced up-regulation of FoxO-mediated transcriptional activity, blocked caspase-3 activation and protected neurones from excitotoxicity. Collectively, this supports the concept that tBHQ and structurally similar antioxidants have potential neuroprotective utility in neurodegeneration, particularly in those conditions linking FoxO activation to oxidative stress and excitotoxic neuronal cell death.

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      Comparative protein interactomics of neuroglobin and myoglobin (pages 192–198)

      Bryan A. Haines, Darcy A. Davis, Artem Zykovich, Botao Peng, Rammohan Rao, Sean D. Mooney, Kunlin Jin and David A. Greenberg

      Article first published online: 14 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07881.x

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      Neuroglobin and Myoglobin InteractomesTo explore mechanisms of neuroglobin-mediated cytoprotection from hypoxia and ischemia, we investigated protein–protein interactions of neuroglobin and myoglobin in normoxic and hypoxic cells. Some interactors were unique to neuroglobin or myoglobin, or to normoxia or hypoxia, whereas others were shared; neuroglobin interactors included anti-oxidative and anti-apoptotic proteins, as well as proteins implicated in neurodegenerative diseases. Protein–protein interactions of neuroglobin may be important for its neuroprotective effects.

  4. OBITUARY

    1. Top of page
    2. REVIEW
    3. SHORT COMMUNICATIONS
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. CORRIGENDUM
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      Richard Burnard Rodnight, 1921–2012 (pages 199–201)

      Peter Dunkley

      Article first published online: 27 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07894.x

  5. CORRIGENDUM

    1. Top of page
    2. REVIEW
    3. SHORT COMMUNICATIONS
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. CORRIGENDUM
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      Corrigendum (page 202)

      Article first published online: 16 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07915.x

      This article corrects:

      Transcriptomic profiles of Wnt3a and insulin in primary cultured rat cortical neurones

      Vol. 118, Issue 4, 512–520, Article first published online: 1 JUL 2011

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