Journal of Neurochemistry

Cover image for Vol. 131 Issue 5

Edited By: Jörg Schulz

Impact Factor: 4.244

ISI Journal Citation Reports © Ranking: 2013: 63/252 (Neurosciences); 74/291 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

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  2. α-synuclein-induced mitochondrial dysfunction in isolated preparation and intact cells: Implications in the pathogenesis of Parkinson's disease

    Aritri Bir, Oishimaya Sen, Shruti Anand, Vineet Kumar Khemka, Priyanjalee Banerjee, Roberto Cappai, Arghyadip Sahoo and Sasanka Chakrabarti

    Article first published online: 18 NOV 2014 | DOI: 10.1111/jnc.12966

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    α-Synuclein is shown to cause mitochondrial impairment through interaction with permeability transition pore complex in isolated preparations. Intracellular accumulation of α-synuclein in SHSY5Y cells following proteasomal inhibition leads to mitochondrial impairment and cell death which could be prevented by knocking down α-synuclein gene. The results link mitochondrial dysfunction and α-synuclein accumulation, two key pathogenic mechanisms of Parkinson's disease, in a common damage pathway.

  3. The effects of nesfatin-1 in the paraventricular nucleus on gastric motility and its potential regulation by the lateral hypothalamic area in rats

    Fei-fei Guo, Luo Xu, Sheng-li Gao, Xiang-rong Sun, Zhi-ling Li and Yan-ling Gong

    Article first published online: 18 NOV 2014 | DOI: 10.1111/jnc.12973

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    Nesfatin-1 regulated the gastric distension (GD)-responsive neurons and reduced gastric motility in the paraventricular nucleus (PVN), which were partly blocked by H4928. Electrical stimulation of the lateral hypothalamic area (LHA) increased the firing activities of GD-responsive neurons in the PVN and promoted the gastric motility. NUCB2/nesfatin-1/fluorogold double-labeled neurons were identified in the LHA, indicating that nesfatin-1 in the PVN could play a pivotal role in the central control of gastric motility and the LHA may participate in the regulatory process. NUCB2 = nucleobindin-2

  4. Differential effects of exercise on brain opioid receptor binding and activation in rats

    Ricardo Mario Arida, Sérgio Gomes da Silva, Alexandre Aparecido de Almeida, Esper Abrão Cavalheiro, Cecilia Zavala-Tecuapetla, Serge Brand and Luisa Rocha

    Article first published online: 17 NOV 2014 | DOI: 10.1111/jnc.12976

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    We characterized the binding and G protein activation of mu, kappa, and delta opioid receptors in several brain regions following acute (7 days) and chronic (30 days) exercise. Higher opioid receptor binding was observed in the acute exercise animal group and opposite findings in the chronic exercise group. Higher G protein activation under basal conditions was noted in rats submitted to chronic exercise, as visible in the depicted pseudo-color autoradiograms.

  5. The anticonvulsant actions of carisbamate associate with alterations in astrocyte glutamine metabolism in the lithium–pilocarpine epilepsy model

    Mussie Ghezu Hadera, Jean-Baptiste Faure, Nina Berggaard, Tesfaye Wolde Tefera, Astrid Nehlig and Ursula Sonnewald

    Article first published online: 17 NOV 2014 | DOI: 10.1111/jnc.12977

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    To understand the metabolic basis of the strong neuroprotection and reduction in seizure severity caused by carisbamate (CRS) in the lithium–pilocarpine (Li-Pilo) model of temporal lobe epilepsy (TLE), we injected CRS for 7 days starting 1 h after status epilepticus and 2 months later [1-13C]glucose and [1,2-13C]acetate. 13C Magnetic resonance spectroscopy analysis was performed on brain extracts and we found that CRS prevented reduction in neuronal mitochondrial metabolism but its effect on astrocytes was likely key in determining outcome of treatment in this model. ALE = absence like epilepsy; acetyl CoA = acetyl coenzyme A; GS = glutamine synthetase; PAG = phosphate activated glutaminase; PC = pyruvate carboxylase; OAA = oxaloacetate; TCA cycle = tricarboxylic acid cycle.