Journal of Neurochemistry
© International Society for Neurochemistry
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
- 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
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.
- 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
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.
- 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
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.
- 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
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.
- The transcription factor Pax6 contributes to the induction of GLT-1 expression in astrocytes through an interaction with a distal enhancer element
Mausam Ghosh, Meredith Lane, Elizabeth Krizman, Rita Sattler, Jeffrey D. Rothstein and Michael B. Robinson
Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13406
The astroglial glutamate transporter GLT-1 shows selective expression in astrocytes and its expression can be induced by neurons. In this study, we demonstrate that Pax6 is expressed in astrocytes and binds to the GLT-1 promoter in vitro and in vivo. Exogenous expression of Pax6 increases GLT-1 and enhanced green fluorescent protein (eGFP) expression in astrocytes from a transgenic mouse line that uses the GLT-1 gene to drive eGFP expression, and an shRNA directed against Pax6 attenuates neuron-dependent induction of GLT-1/eGFP. We therefore conclude that Pax6 contributes to the neuron-dependent induction of GLT-1.