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Journal of Neurochemistry

Cover image for Vol. 121 Issue 3

May 2012

Volume 121, Issue 3

Pages 327–494

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
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  2. REVIEW

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. You have full text access to this OnlineOpen article
      Purine nucleosides: endogenous neuroprotectants in hypoxic brain (pages 329–342)

      Bettina Thauerer, Stephanie zur Nedden and Gabriele Baier-Bitterlich

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07692.x

  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
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      Cdk5/p35 phosphorylates lemur tyrosine kinase-2 to regulate protein phosphatase-1C phosphorylation and activity (pages 343–348)

      Catherine Manser, Alessio Vagnoni, Florence Guillot, Jennifer Davies and Christopher C. J. Miller

      Article first published online: 10 APR 2012 | DOI: 10.1111/j.1471-4159.2012.07650.x

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      Lemur tyrosine kinase-2 links cdk5/p35 to protein phosphatase-1 and downstream targets such as GSK3β. Cdk5/p35 is a kinase that regulates a variety of neuronal functions. One route whereby it fulfils these functions is by inducing the inhibitory phosphorylation of protein phosphatase-1C, which then signals to downstream targets such as GSK3β. In this issue, Manser et al. demonstrate that cdk5/p35-mediated phosphorylation of PP1C involves lemur tyrosine kinase-2. Cdk5/p35 phosphorylates LMTK2 to stimulate LMTK2 phosphorylation of PP1C.

  4. ORIGINAL ARTICLES

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

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      Modulation of recombinant, α2*, α3* or α4*-nicotinic acetylcholine receptor (nAChR) function by nAChR β3 subunits (pages 349–361)

      Bhagirathi Dash, Minoti Bhakta, Yongchang Chang and Ronald J. Lukas

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07685.x

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      nAChR β3 subunits affects agonist sensitivity and efficacy; and rates of receptor desensitization to various degrees Natural incorporation of β3 subunits could occur into various nAChR subtypes. Such incorporation is shown to have modest effects on sensitivity to endogenous ACh or exogenous nicotine; a milder negative effect on levels of nAChR function, the exceptions being a larger negative effect on α3β2*- and α4β2-*-nAChR; and mostly an undistinguishable effect on rates of desensitization. These data could be relevant for developing therapeutics for treatment of nicotine addiction.

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      Activation of phospholipase-Cγ and protein kinase C signal pathways helps the survival of spinal motoneurons injured by root avulsion (pages 362–372)

      Xiu-Chun Zhao, Lin-Lin Wang, Ya-Qiong Wang, Fa-Huan Song, Ying-Qin Li, Rao Fu, Wen-Hua Zheng, Wutian Wu and Li-Hua Zhou

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07696.x

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      Brachial root-avulsion leads to hand paralysis because of the death of injured spinal motoneurons, but the intracellular molecular events are uncertain. Here, we demonstrate that PLCγ/PKC/nNOS signal molecules are activated inside injured motoneurons after injury; furthermore, PLCγ mediates, while PKC and nNOS are associated with, avulsion-induced spinal motoneuron death. We believe that understanding the intracellular signaling mechanism is essential for developing therapies to rescue the motoneurons from the root-avulsion of the brachial plexus.

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      Kv7 (KCNQ) channel openers normalize central 2-deoxyglucose uptake in a mouse model of mania and increase prefrontal cortical and hippocampal serine-9 phosphorylation levels of GSK3β (pages 373–382)

      Line V. Kristensen, Karin Sandager-Nielsen and Henrik H. Hansen

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07704.x

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      Anti-manic efficacy of Kv7 channel openers There is a great need for identifying new agents targeting molecular mechanisms involved in the pathophysiology of bipolar disorder. Kv7 (KCNQ) channel openers mimic several features of mood stabilizers by reducing baseline cerebral 2-deoxyglucose metabolic activity, preventing CNS hypermetabolic activity in a mouse model of mania, and increasing cerebral GSK3β serine-9 phosphorylation. Consequently, Kv7.2/Kv7.3 channels may present a novel anti-manic therapeutic target.

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      Characterization of the Drosophila adenosine receptor: the effect of adenosine analogs on cAMP signaling in Drosophila cells and their utility for in vivo experiments (pages 383–395)

      Lucie Kucerova, Vaclav Broz, Jana Fleischmannova, Eva Santruckova, Roman Sidorov, Vladimir Dolezal and Michal Zurovec

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07701.x

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      Schematic interactions of agonists with A2AR/DmAdoR To understand the complexity of adenosine responses, we established a pharmacological profile of the only known Drosophila adenosine receptor (DmAdoR). The DmAdoR in Drosophila cells induced cAMP but not intracellular calcium. The utility of the DmAdoR agonist CADO and antagonist SCH58261 were examined in flies in vivo. Our results constitute a necessary background for understanding the evolution of adenosine signaling.

    5. Bioenergetics & Metabolism

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      Characterization of cerebral glucose dynamics in vivo with a four-state conformational model of transport at the blood–brain barrier (pages 396–406)

      João M. N. Duarte and Rolf Gruetter

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07688.x

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      The present study shows that a four-state conformational model allows reliable determination of kinetics of both glucose uptake and consumption upon dynamic simultaneous measurement of plasma and brain glucose concentration changes. This method can therefore be an alternative to other non-invasive standard methods to determine glucose uptake and consumption that mostly relied on the utilization of isotope-enriched glucose or glucose analogs.

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      Effects of acute and chronic hyperglycemia on the neurochemical profiles in the rat brain with streptozotocin-induced diabetes detected using in vivo1H MR spectroscopy at 9.4 T (pages 407–417)

      Wen-Tung Wang, Phil Lee, Hung-Wen Yeh, Irina V. Smirnova and In-Young Choi

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07698.x

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      The cerebral metabolic consequences of untreated hyperglycemia from the onset to the chronic stage were studied in an animal model of diabetes using in vivo1H-MRS. Acute hyperglycemia increased brain glucose, osmolytes and ketone bodies. Chronic hyperglycemia reduced NAA and glutathione levels. Irreversible alterations of neurochemical levels by glycemic normalization indicate the impact of prolonged uncontrolled hyperglycemia on the CNS.

    7. Neuroinflammation & Neuroimmunology

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      The cyclooxygenase-2 pathway via the PGE2 EP2 receptor contributes to oligodendrocytes apoptosis in cuprizone-induced demyelination (pages 418–427)

      Sara Palumbo, Christopher D. Toscano, Laura Parente, Roberto Weigert and Francesca Bosetti

      Article first published online: 18 JUL 2011 | DOI: 10.1111/j.1471-4159.2011.07363.x

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      Multiple sclerosis (MS) is a human demyelinating disease characterized by oligodendrocyte cell death. Although the enzyme cyclooxygenase (COX)-2 has been suggested to be involved in the pathogenesis of MS, little is known about the direct involvement of COX-2/PGE2/EP pathway in myelin and oligodendrocyte injury. Hence, the present study investigates the role of COX-2/EP signaling in the pathogenesis of primary demyelination using the well-characterized cuprizone model. Immunohistochemical analyses revealed selective increases in both COX-2 and EP2 receptor expression in oligodendrocytes after cuprizone exposure that preceded histological demyelination. Further, COX-2 gene deletion or selective pharmacological inhibition of either COX-2 or EP2 attenuated the apoptotic death of oligodendrocytes, as well as, the subsequent demyelination and motor dysfunction that follows cuprizone treatment. Together, these data demonstrate that the involvement of COX-2 in the pathogenesis of cuprizone-induced demyelination occurs via PGE2 EP2 receptor-mediated initiation of oligodendrocyte apoptosis.

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      RANTES-mediated control of excitatory amino acid release in mouse spinal cord (pages 428–437)

      Silvia Di Prisco, Maria Summa, Vineetha Chellakudam, Pia Irene Anna Rossi and Anna Pittaluga

      Article first published online: 21 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07720.x

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      RANTES-mediated effects on glutamate release from mouse spinal cord terminals was investigated and compared with those observed in the cortex. RANTES-induced modulation of glutamate release occurred in an area-specific manner, involving different receptor repertoires. RANTES-induced effects could be observed in healthy tissue, suggesting that the events here described could participate to the chemokine-mediated neuroprotective processes in CNS.

    9. Molecular Basis of Disease

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      Cytosolic acidification and intracellular zinc release in hippocampal neurons (pages 438–450)

      Lech Kiedrowski

      Article first published online: 15 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07695.x

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      Cytosolic acidification induces intracellular Zn2+ release in hippocampal neurons. This study was performed to clarify the mechanism of glutamate-induced and Ca2+-dependent intracellular Zn2+ release. A cytosolic pH drop caused by Ca2+ influx via NMDA receptors was found to trigger intracellular Zn2+ release. The data suggest that an analogous intracellular Zn2+ release may take place in the brain during ischemic acidosis.

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      Cynandione A mitigates ischemic injuries in rats with cerebral ischemia (pages 451–464)

      Rongcai Yue, Xing Yuan, Xiaojun Liu, Jigang Zhang, Peng Jiang, Cheng He, Lei Shan, Yizhi Yu and Weidong Zhang

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07682.x

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      Cynandione A mitigates ischemic injuriesCynandione A possesses potent antioxidant activities and shows neuroprotective actions both in vitro and in rats with transient focal cerebral ischemia. Cynandione A suppresses DPYSL2 cleavage and antagonizes the rises in HMGB1 levels in the brain tissues of ischemic rats, which could contribute to the neuroprotective properties. Cynandione A should be further explored as a neuroprotective agent for ischemic stroke.

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      Spinal muscular atrophy pathogenic mutations impair the axonogenic properties of axonal-survival of motor neuron (pages 465–474)

      Denise Locatelli, Paolo d’Errico, Silvia Capra, Adele Finardi, Francesca Colciaghi, Veronica Setola, Mineko Terao, Enrico Garattini and Giorgio Battaglia

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07689.x

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      Mutated ha-SMN proteins impair axonogenesis Axonal-SMN is a truncated isoform of SMN1, the disease gene for spinal muscular atrophy or SMA. We demonstrated here that SMA pathogenic mutations affect a-SMN function in stimulating axon growth. Mutated a-SMN proteins induce the growth of shorter axons with prominent morphologic abnormalities. Our data represent the first indication possibly linking a-SMN loss of function to SMA pathogenesis.

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      A novel variant of human superoxide dismutase 1 harboring amyotrophic lateral sclerosis-associated and experimental mutations in metal-binding residues and free cysteines lacks toxicity in vivo (pages 475–485)

      Mercedes Prudencio, Herman Lelie, Hilda H. Brown, Julian P. Whitelegge, Joan S. Valentine and David R. Borchelt

      Article first published online: 20 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07690.x

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      Intragenic suppressor mutations of SOD1 in vivo toxicity Does metal-binding by Cu/Zn SOD1 influences its toxicity in dominantly inherited motor neuron disease? Combining disease-associated and experimental mutations in histidine and cysteine residues that bind Cu/Zn produced a non-toxic variant of SOD1 (SODMD). In cell culture, the combined C6G and C111S mutations of SODMD protein dramatically reduced its propensity to aggregate and may account for its lack of toxicity.

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      Changes in 20S subunit composition are largely responsible for altered proteasomal activities in experimental autoimmune encephalomyelitis (pages 486–494)

      Jianzheng Zheng, Anushka Dasgupta and Oscar A. Bizzozero

      Article first published online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07699.x

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      Changes in proteasome and immunoproteasome expression during inflammatory demyelination. Previously, we have shown that the various proteasome peptidase activities are altered in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. In this study, we demonstrate that those changes are the result of fluctuations in the amount of the catalytic subunits of the immunoproteasome (i-20S) and standard proteasome (s-20S), both of which can efficiently hydrolyze carbonylated proteins. These findings suggest that build-up of oxidized proteins in chronic EAE is the result of decreased s-20S expression. In contrast, augmented protein oxidation in acute EAE is compensated by increased i-20S expression.

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