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Journal of Neurochemistry

Cover image for Journal of Neurochemistry

January 2013

Volume 124, Issue 1

Pages 1–158

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. ORIGINAL ARTICLES
    4. CORRIGENDUM
    1. You have free access to this content
      Apolipoprotein E acts at pre-synaptic sites… among others (pages 1–3)

      Steven W. Barger

      Article first published online: 28 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07935.x

      Read the full article ‘APOE genotype affects the pre-synaptic compartment of glutamatergic nerve terminals’ on doi: 10.1111/j.1471-4159.2012.07908.x.

  2. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. ORIGINAL ARTICLES
    4. CORRIGENDUM
    1. Signal Transduction & Synaptic Transmission

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      APOE genotype affects the pre-synaptic compartment of glutamatergic nerve terminals (pages 4–14)

      Sonya B. Dumanis, Amanda M. DiBattista, Matthew Miessau, Charbel E. H. Moussa and G. William Rebeck

      Article first published online: 28 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07908.x

      Thumbnail image of graphical abstract

      Using human APOE knock-in mice, we found that APOE genotype affected pre-synaptic components in normal brain. Specifically, APOE-ε4 TR mice had decreased glutaminase levels and increased levels of the vesicular glutamate transporter VGLUT1. Using high-frequency 13C/1H nuclear magnetic resonance spectroscopy, we found that APOE-ε4TR mice have decreased production of glutamate and increased levels of glutamine.

      Read the Editorial Highlight for this article on doi: 10.1111/j.1471-4159.2012.07935.x.

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      Synaptosomes secrete and uptake functionally active microRNAs via exocytosis and endocytosis pathways (pages 15–25)

      Jie Xu, Qun Chen, Ke Zen, Chenyu Zhang and Qipeng Zhang

      Article first published online: 21 NOV 2012 | DOI: 10.1111/jnc.12057

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      Synaptic miRNAs are existed in synapse and regulate the local translation within the synapse. In present study, Jie-Xu et al. found that miRNAs were existed in synaptic vesicles and could be secreted or uptaken via exocytosis and endocytic pathways. This new finding for first time demonstrated the secretion of miRNAs by synaptosomes under physiological stimulation and the secreted miRNAs might be functionally active.

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      SMRT-mediated co-shuttling enables export of class IIa HDACs independent of their CaM kinase phosphorylation sites (pages 26–35)

      Francesc X. Soriano, Sangeeta Chawla, Paul Skehel and Giles E. Hardingham

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12058

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      Nuclear export of repressors is an important mechanism of transcriptional regulation. Class IIa HDACs are known to exit the nucleus in Ca2+ dependent manner by CaM Kinase-dependent phosphorylation (a). Here we uncover, in cortical neurons, a novel mechanism of class IIa HDAC nuclear export which is independent of CaM Kinase-dependent phosphorylation, mediated by co-shuttling with co-repressor SMRT. SMRT's class IIa HDAC-interacting domain RD3 is key for co-shuttling (b). We go on to show that this finding is physiologically relevant in the BDNF signaling (c). We find that BDNF promotes the direct nuclear import of HDAC5, but the nuclear export of SMRT. The effect of SMRT-mediated HDAC5 co-shuttling means that the presence of SMRT effectively prevents BDNF-induced direct HDAC5 import. (a) Phospho-mutant forms of class IIa HDACs cannot be exported by Ca2+ signals. (b) SMRT renders phospho-mutant forms of HDACs exportable by Ca2+ signals. (c) SMRT-mediated HDAC5 export opposes BDNF-induced HDAC5 nuclear accumulation.

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      The C-terminal domain of tetanus toxin protects motoneurons against acute excitotoxic damage on spinal cord organotypic cultures (pages 36–44)

      Mireia Herrando-Grabulosa, Caty Casas and José Aguilera

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12062

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      One of the main processes that induces motoneuron (MN) cell death is the excitotocity triggered after Spinal Cord Injury (SCI). C-terminal domain of tetanus toxin (Hc-TeTx domain) protects motoneurons against this damage by activating several pro-survival signalling pathways, such as autophagy. Hc-TeTx could be useful as a neuroprotector agent to promotes MN survival.

    5. Neuroinflammation & Neuroimmunology

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      S-nitrosylated protein disulfide isomerase contributes to mutant SOD1 aggregates in amyotrophic lateral sclerosis (pages 45–58)

      Xueping Chen, Xiaosha Zhang, Chen Li, Teng Guan, Huifang Shang, Liying Cui, Xin-Min Li and Jiming Kong

      Article first published online: 1 NOV 2012 | DOI: 10.1111/jnc.12046

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      We proposed a role of nitrosative stress in the formation of SOD1 aggregates in transgenic mice expressing mutant SOD1: inducible nitric oxide synthase up-regulation generates high levels of nitric oxide and subsequently induces S-nitrosylation of PDI, leading to SOD1 misfolding and aggregation. Our findings suggest that PDI should be a target for new therapeutic strategies for ALS.

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      Cyclooxygenase-1 inhibition reduces amyloid pathology and improves memory deficits in a mouse model of Alzheimer's disease (pages 59–68)

      Sang-Ho Choi, Saba Aid, Luca Caracciolo, S. Sakura Minami, Takako Niikura, Yasuji Matsuoka, R. Scott Turner, Mark P. Mattson and Francesca Bosetti

      Article first published online: 21 NOV 2012 | DOI: 10.1111/jnc.12059

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      The role of COX-1 in AD has not been considered carefully in part due to the presumed predominant role of COX-2 in neuroinflammation. Here we show that the COX-1 inhibitor SC-560 reduces amyloid deposits and improves memory deficits in 3 × Tg-AD mice. These results suggest that COX-1 should be further considered as a potential target for therapeutic intervention.

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      Microglial and astroglial activation by 3,4-methylenedioxymethamphetamine (MDMA) in mice depends on S(+) enantiomer and is associated with an increase in body temperature and motility (pages 69–78)

      Lucia Frau, Nicola Simola, Antonio Plumitallo and Micaela Morelli

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12060

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      MDMA is an amphetamine derivative with rewarding properties that can also induce neuroinflammation and neurodegeneration. Since two enantiomers of MDMA exist, it is fundamental to know the relative efficacy of each of them. This study demonstrates that S(+)-MDMA is the main responsible of the neuroinflammatory effects of racemic MDMA. The results underline the importance of studying chirality in MDMA-induced neurotoxicity and neuroinflammation.

    8. Neuronal Plasticity & Behavior

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      Sleep/wake dependent changes in cortical glucose concentrations (pages 79–89)

      Michael B Dash, Michele Bellesi, Giulio Tononi and Chiara Cirelli

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12063

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      The brain overwhelmingly relies on glucose to meet its energy needs, which are higher in wake and REM sleep than in NREM sleep, but it remains unclear how the extracellular concentration of glucose [gluc] changes during sleep and wake. Using fixed-potential amperometry we find that in rat cerebral cortex [gluc] increases progressively during NREM sleep, decreases progressively during REM sleep, and initially declines (~8 min) before increasing during wake. Surprisingly, the early glucose decline upon awakening is longer after prolonged wake than after consolidated sleep, suggesting that sleep/wake history may affect brain glucose availability.

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      Nesfatin-1, corticotropin-releasing hormone, thyrotropin-releasing hormone, and neuronal histamine interact in the hypothalamus to regulate feeding behavior (pages 90–99)

      Koro Gotoh, Takayuki Masaki, Seiichi Chiba, Hisae Ando, Takanobu Shimasaki, Kimihiko Mitsutomi, Kansuke Fujiwara, Isao Katsuragi, Tetsuya Kakuma, Toshiie Sakata and Hironobu Yoshimatsu

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12066

      Thumbnail image of graphical abstract

      Nesfatin-1, corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and hypothalamic neuronal histamine act as anorexigenics in the hypothalamus. Nesfatin-1 increased CRH and TRH levels and histamine turnover, whereas histamine also increased nesfatin-1 level in the hypothalamus. These results indicate that CRH, TRH and hypothalamic neuronal histamine mediate the suppressive effects of nesfatin-1 on feeding behavior.

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      Unique gene alterations are induced in FACS-purified Fos-positive neurons activated during cue-induced relapse to heroin seeking (pages 100–108)

      Sanya Fanous, Danielle H. Guez-Barber, Evan M. Goldart, Regina Schrama, Florence R. M. Theberge, Yavin Shaham and Bruce T. Hope

      Article first published online: 21 NOV 2012 | DOI: 10.1111/jnc.12074

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      Unique gene expression in neurons activated during cue-induced heroin seeking

      Learned associations during heroin self-administration are encoded within neuronal ensembles that can be selectively activated by drug-related cues. We used fluorescent-activated cell-sorting (FACS) to purify activated Fos-positive and non-activated Fos-negative neurons from prefrontal cortex 90 min after heroin seeking under extinction conditions. mRNA levels of the immediate early genes fosB, arc, egr1, and egr2, as well as npy and map2k6, were increased in Fos-positive, but not Fos-negative, neurons. Our data indicate that cue-induced relapse to heroin seeking after prolonged withdrawal induces unique molecular alterations within activated PFC neurons that are distinct from those observed in the surrounding majority of non-activated neurons.

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      Protease-activated receptor-1 modulates hippocampal memory formation and synaptic plasticity (pages 109–122)

      Antoine G. Almonte, Laura H. Qadri, Faraz A. Sultan, Jennifer A. Watson, Daniel J. Mount, Gavin Rumbaugh and J. David Sweatt

      Article first published online: 21 NOV 2012 | DOI: 10.1111/jnc.12075

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      PAR1 is an intriguing GPCR that is activated by proteolytic cleavage of its amino terminus by serine proteases; very little is known, however, about PAR1 in normal brain function. We show that PAR1 knockout mice have deficits in a hippocampus-dependent learning and memory behavioral test, and have severe deficits in NMDAR-dependent LTP. Our results suggest an important role for PAR1 function in NMDAR-dependent processes subserving memory formation and synaptic plasticity.

    12. Molecular Basis of Disease

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      APP independent and dependent effects on neurite outgrowth are modulated by the receptor associated protein (RAP) (pages 123–132)

      Andrew J. Billnitzer, Irina Barskaya, Cailing Yin and Ruth G. Perez

      Article first published online: 15 NOV 2012 | DOI: 10.1111/jnc.12051

      Thumbnail image of graphical abstract

      This study was performed to characterize the contributions of APP, sAPPα, LRP, and RAP on neurite outgrowth. Our data reveal that sAPPα alters neuronal morphology, and that ERK modulates RAP effects on neurite outgrowth, especially in the absence of APP. The results suggest that successful AD therapies should preserve protein interactions in order to sustain the synaptic connections underlying memory.

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      Calpain inhibitor attenuated optic nerve damage in acute optic neuritis in rats (pages 133–146)

      Arabinda Das, M. Kelly Guyton, Amena Smith, Gerald Wallace IV, Misty L. McDowell, Denise D. Matzelle, Swapan K. Ray and Naren L. Banik

      Article first published online: 22 NOV 2012 | DOI: 10.1111/jnc.12064

      Thumbnail image of graphical abstract

      Optic Neuritis (ON) is one of the leading indicators of MS progression. Previous work has implicated calpain as a mediator of cell death and disease progression in ON. The current study shows that calpain inhibition by calpeptin attenuates cell death, axonal degeneration, and inflammatory cytokine production. Calpeptin treatment also promotes neuroprotective pathway activation, and thus, it may impede ON progression.

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      The metal transporter SMF-3/DMT-1 mediates aluminum-induced dopamine neuron degeneration (pages 147–157)

      Natalia VanDuyn, Raja Settivari, Jennifer LeVora, Shaoyu Zhou, Jason Unrine and Richard Nass

      Article first published online: 21 NOV 2012 | DOI: 10.1111/jnc.12072

      Thumbnail image of graphical abstract

      Aluminum exposure is a risk factor for Parkinson's disease and Alzheimer's disease, yet the molecular basis for intracellular Al transport and neurotoxicity is poorly defined. We developed a novel model for aluminum-induced dopamine neuron degeneration and provide the first molecular evidence of an animal aluminum transporter. This novel genetic model should facilitate the identification of molecular pathways and potential therapeutic targets involved in Al-associated DA neuron degeneration. Graphical abstract designed by Richard Nass and Albert William.

  3. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. ORIGINAL ARTICLES
    4. CORRIGENDUM
    1. You have free access to this content
      Corrigendum (page 158)

      Article first published online: 12 OCT 2012 | DOI: 10.1111/jnc.12042

      This article corrects:

      Poster abstracts

      Vol. 122, Issue Supplement s1, 11–33, Article first published online: 10 SEP 2012

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