Journal of Neurochemistry

Cover image for Vol. 135 Issue 5

Edited By: Jörg Schulz

Impact Factor: 4.281

ISI Journal Citation Reports © Ranking: 2014: 55/252 (Neurosciences); 72/289 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. Remarkable impairment of Wnt/β-catenin signaling in the brains of the mice infected with scrapie agents

    Jing Sun, Hui Wang, Li-Na Chen, Jing Wang, Yan Lv, Xiao-Dong Yang, Bao-Yun Zhang, Chan Tian, Qi Shi and Xiao-Ping Dong

    Article first published online: 25 NOV 2015 | DOI: 10.1111/jnc.13416

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    Schematic for the impairment of canonical Wnt signaling during prion infection. The left and right parts represent the normal and prion-infected situations, respectively. Prion infection or PrPSc accumulation triggers the over-expression of Dickkopf WNT signaling pathway inhibitor 1 (DKK-1) and the enhancement of glycogen synthase kinase 3β (GSK-3β) activity, which subsequently promotes the phosphorylation and degradation of β-catenin. As a result, the impairment of β-catenin signaling leads to the down-regulation of Wnt target genes.

  2. No improvement of neuronal metabolism in the reperfusion phase with melatonin treatment after hypoxic-ischemic brain injury in the neonatal rat

    Hester R. Berger, Tora Sund Morken, Riyas Vettukattil, Ann-Mari Brubakk, Ursula Sonnewald and Marius Widerøe

    Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13420

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    Neuronal and astrocytic metabolism was examined by 13C and 1H NMR spectroscopy in the early reperfusion phase after unilateral hypoxic-ischemic brain injury and melatonin treatment in neonatal rats. One hour after hypoxia-ischemia astrocytic mitochondrial metabolism had recovered and glycolysis was normalized, whereas mitochondrial metabolism in neurons was impaired. Melatonin treatment did not show a protective effect on neuronal metabolism.

  3. Striatal adenosine–cannabinoid receptor interactions in rats over-expressing adenosine A2A receptors

    Valentina Chiodi, Antonella Ferrante, Luca Ferraro, Rosa Luisa Potenza, Monica Armida, Sarah Beggiato, Antonella Pèzzola, Michael Bader, Kjell Fuxe, Patrizia Popoli and Maria Rosaria Domenici

    Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13421

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    We studied A2A-CB1 receptor interaction in transgenic rats over-expressing adenosine A2A receptors under the control of the neuron-specific enolase promoter (NSEA2A). In these rats, we demonstrated a reduced effect of the CB1 receptor agonist WIN 55,212-2 in the modulation of corticostriatal synaptic transmission and locomotor activity, while CB1 receptor expression level did not change with respect to WT rats. A reduction in the expression of A2A-CB1 receptor heteromers is postulated.

  4. Mitochondrial and lysosomal biogenesis are activated following PINK1/parkin-mediated mitophagy

    Davor Ivankovic, Kai-Yin Chau, Anthony H. V. Schapira and Matthew E. Gegg

    Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13412

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    Damaged mitochondria are degraded by the autophagy–lysosome pathway and is termed mitophagy. Following mitophagy induction, the transcription factors Nrf2 and TFEB translocate to the nucleus, inducing the transcription of genes encoding for autophagic proteins such as p62, as well as lysosomal and mitochondrial proteins. We propose that these events maintain autophagic flux, replenish lysosomes and replace mitochondria.

  5. Chronic and progressive Parkinson's disease MPTP model in adult and aged mice

    Ana B. Muñoz-Manchado, Javier Villadiego, Sonia Romo-Madero, Nela Suárez-Luna, Alfonso Bermejo-Navas, José A. Rodríguez-Gómez, Pablo Garrido-Gil, José L. Labandeira-García, Miriam Echevarría, José López-Barneo and Juan J. Toledo-Aral

    Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13409

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    Here, we show a new chronic and progressive parkinsonian mouse model, in young and aged mice. This model produces a stable degeneration of the dopaminergic nigrostriatal pathway, continuous neuroinflammatory reaction and motor deficits. Aged animals showed a faster neurodegeneration and an altered neuroinflammatory response. This treatment could be useful to model different stages of PD and to test both protective and restorative therapeutic approaches.