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Journal of Neurochemistry

Cover image for Vol. 120 Issue 3

February 2012

Volume 120, Issue 3

Pages 347–473

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTILCES
    4. ORIGINAL ARTICLES
    5. ADDENDUM
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  2. REVIEW ARTILCES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTILCES
    4. ORIGINAL ARTICLES
    5. ADDENDUM
    1. You have free access to this content
      Cross-functional E3 ligases Parkin and C-terminus Hsp70-interacting protein in neurodegenerative disorders (pages 350–370)

      Pravir Kumar, Kaveri Pradhan, R. Karunya, Rashmi K. Ambasta and Henry W. Querfurth

      Version of Record online: 21 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07588.x

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      Structural contributions of antipsychotic drugs to their therapeutic profiles and metabolic side effects (pages 371–384)

      Somayeh Jafari, Francesca Fernandez-Enright and Xu-Feng Huang

      Version of Record online: 15 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07590.x

  3. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTILCES
    4. ORIGINAL ARTICLES
    5. ADDENDUM
    1. Signal Transduction & Synaptic Transmission

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      Aberrant striatal dopamine transmitter dynamics in brain-derived neurotrophic factor-deficient mice (pages 385–395)

      Kelly E. Bosse, Francis K. Maina, Johnna A. Birbeck, Marion M. France, Joseph J. P. Roberts, Michelle L. Colombo and Tiffany A. Mathews

      Version of Record online: 2 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07531.x

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      Endogenous BDNF influences dopamine system homeostasis. The effect of low endogenous levels of brain-derived neurotrophic factor (BDNF) on dopamine system function was characterized in the caudate-putamen of heterozygous BDNF (BDNF+/−) mice. BDNF+/− mice had significantly elevated basal and potassium-stimulated extracellular dialysate dopamine levels compared to wildtype mice. Endogenous BDNF influences dopamine system homeostasis by regulating the release and uptake dynamics of pre-synaptic dopamine transmission as measured by voltammetry.

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      Clozapine functions through the prefrontal cortex serotonin 1A receptor to heighten neuronal activity via calmodulin kinase II–NMDA receptor interactions (pages 396–407)

      Sudarshana Purkayastha, Jason Ford, Baishali Kanjilal, Souleymane Diallo, Joseph Del Rosario Inigo, Lorenz Neuwirth, Abdeslem El Idrissi, Zaghloul Ahmed, Andrzej Wieraszko, Efrain C. Azmitia and Probal Banerjee

      Version of Record online: 15 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07565.x

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      How clozapine worksNerve signals in the analytical center of the brain prefrontal cortex (PFC) are impaired in Schizophrenia but how the therapeutic agent clozapine normalizes these signals is unknown. This study analyzes nerve signals and molecular interactions in the PFC to explain how clozapine works. Our findings unify multiple prior hypotheses into one mechanistic model for the action of clozapine.

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      The Discoidin domain receptor 1 gene has a functional A2RE sequence (pages 408–418)

      Barbara Roig, Sílvia Moyano, Lourdes Martorell, Javier Costas and Elisabet Vilella

      Version of Record online: 6 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07580.x

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      DDR1 is a human myelin protein. Intracellular trafficking of myelin mRNAs containing A2RE sequence has been described in human oligodendrocytes. Here, we identified an A2RE-like sequence in human DDR1 mRNA. DDR1 A2RE sequence contains a SNP rs2267641 which influences brain mRNA expression of DDR1b and DDR1c isoforms. Silencing hnRNP A2/B1 RNA in oligodendroglial HOG16 cells differentially alters DDR1mRNA expression and decreases DDR1 protein expression. These results evidence the direct implication of hnRNP A2/B1 in DDR1 splicing process and intracellular trafficking of DDR1 mRNA to the olidendrocyte cytoplasmic edges.

    4. Molecular Basis of Disease

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      Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer’s disease (pages 419–429)

      Baiyang Sheng, Xinglong Wang, Bo Su, Hyoung-gon Lee, Gemma Casadesus, George Perry and Xiongwei Zhu

      Version of Record online: 8 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07581.x

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      Mitochondrial biogenesis is regulated by the PGC-1α-NRF-TFAM pathway. We found decreased expression of these molecules in both AD hippocampal tissues and APPswe M17 cells. PGC-1α over-expression could completely rescue while PGC-1α knockdown could exacerbate impaired mitochondrial biogenesis and mitochondrial deficits in APPswe cells. Furthermore, the PKA/CREB pathway plays a critical role in the regulation of PGC-1α expression in APPswe cells.

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      Pin1 inhibition activates cyclin D and produces neurodegenerative pathology (pages 430–439)

      Kutay Deniz Atabay and Arzu Karabay

      Version of Record online: 5 MAY 2011 | DOI: 10.1111/j.1471-4159.2011.07259.x

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      α-Synuclein oligomers oppose long-term potentiation and impair memory through a calcineurin-dependent mechanism: relevance to human synucleopathic diseases (pages 440–452)

      Zane S. Martin, Volker Neugebauer, Kelly T. Dineley, Rakez Kayed, Wenru Zhang, Lindsay C. Reese and Giulio Taglialatela

      Version of Record online: 28 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07576.x

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      Reversing the cognitive effects of the Parkinson’s disease protein alpha synucleinThe present study was performed to investigate neuronal and behavioral effects elicited by small aggregates (oligomers) of α-synuclein, the toxic protein present in the brain of patients affected by severe neurological disorders such as Parkinson’s disease and dementia with Lewy bodies. We found that extracellularly delivered α-synuclein oligomers profoundly affect neuronal function and induce acute memory deficits that occurred independently of neuronal death and that could be reversed by inhibiting a specific neuronal enzyme. Notably, evidence of such an effect could be also observed in actual diseased human brain specimens. These novel results illustrate that some cognitive impairments normally seen in human neurological diseases involving α-synuclein precede overt neuronal death and suggest an effective pharmacological target to treat them, possibly delaying further progression of the disease.

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      Hypoxia inducible factor-1α is involved in the neurodegeneration induced by isoflurane in the brain of neonatal rats (pages 453–460)

      Hong Jiang, Yan Huang, Hui Xu, Yu Sun, Ning Han and Qi Fang Li

      Version of Record online: 15 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07589.x

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      Volatile anesthetic induced neurodegeneration via HIF-1α Isoflurane induces neurodegenration by an unknown mechanism. We reported isoflurane up-regulates HIF-1α expression in vivo and in vitro during induction of neurodegeneration. Furthermore, knockdown of HIF-1α expression in cultured neurons attenuated isoflurane-induced neurotoxicity. Hence, anesthetic agents like isoflurane should be carefully evaluated and probably used with caution when anesthetizing pediatric patients.

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      Resveratrol mitigates lipopolysaccharide- and Aβ-mediated microglial inflammation by inhibiting the TLR4/NF-κB/STAT signaling cascade (pages 461–472)

      Hemachander Capiralla, Valérie Vingtdeux, Haitian Zhao, Roman Sankowski, Yousef Al-Abed, Peter Davies and Philippe Marambaud

      Version of Record online: 16 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07594.x

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      Anti-inflammatory effect of resveratrol: Can it help with Alzheimer's disease? Resveratrol is a natural polyphenol associated with anti-inflammatory properties and currently in clinical trials for Alzheimer’s disease. Here, we show that resveratrol efficiently prevents in vitro in cell lines and in vivo in mice the pro-inflammatory response of microglial cells triggered by the amyloid-β peptide. This work provides support for the beneficial effect of resveratrol intake against Alzheimer’s disease pathogenesis.

  4. ADDENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTILCES
    4. ORIGINAL ARTICLES
    5. ADDENDUM
    1. You have free access to this content
      Quality control parameters on a large dataset of regionally dissected human control brains for whole genome expression studies (page 473)

      Daniah Trabzuni, Mina Ryten, Robert Walker, Colin Smith, Sabaena Imran, Adaikalavan Ramasamy, Michael Weale and John Hardy

      Version of Record online: 7 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07602.x

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