Journal of Neurochemistry

Cover image for Vol. 134 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. You have full text access to this OnlineOpen article
    Identification of long noncoding RNAs dysregulated in the midbrain of human cocaine abusers

    Michael J. Bannon, Candace L. Savonen, Hui Jia, Fabien Dachet, Steven D. Halter, Carl J. Schmidt, Leonard Lipovich and Gregory Kapatos

    Article first published online: 1 SEP 2015 | DOI: 10.1111/jnc.13255

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    Long noncoding RNAs (lncRNAs) regulate the expression of protein-coding genes, but little is known about their potential role in drug abuse. In this study, we identified lncRNAs differentially expressed in human cocaine abusers' midbrains. One up-regulated antisense lncRNA, tumor necrosis factor receptor-associated factor 3-interacting protein 2-antisense 1 (TRAF3IP2-AS1), was found predominantly in the nucleus of human dopamine (DA) neurons, whereas the related TRAF3IP2 protein-coding transcript was distributed throughout these cells. The abundances of these transcripts were significantly correlated (left) suggesting that TRAF3IP2-AS1 may regulate TRAF3IP2 gene expression, perhaps through local chromatin changes at this locus (right).

  2. Activation of the phosphatidylinositol 3-kinase pathway plays important roles in reduction of cerebral infarction by cilnidipine

    Jeong-Woo Son, Hojin Choi, Arum Yoo, Hyun-Hee Park, Young-Seo Kim, Kyu-Yong Lee, Young Joo Lee and Seong-Ho Koh

    Article first published online: 31 AUG 2015 | DOI: 10.1111/jnc.13254

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    We investigated whether cilnidipine has neuroprotective effects on ischemic stroke in an animal model. We have demonstrated that the neuroprotective effect of cilnidipine is associated with the activation of the PI3K pathway. Considering the daily use of antihypertensive drugs for patients with hypertension, cilnidipine could be beneficial for patients with ischemic stroke.

  3. Reduction in NPY-positive neurons and dysregulation of excitability in young senescence-accelerated mouse prone 8 (SAMP8) hippocampus precede the onset of cognitive impairment

    Erika Sawano, Kanako Iwatani, Keiko Tominaga-Yoshino, Akihiko Ogura and Tomoko Tashiro

    Article first published online: 31 AUG 2015 | DOI: 10.1111/jnc.13274

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    Senescence-accelerated mouse prone 8 (SAMP8) shows marked hyperactivity and reduced anxiety before the onset of cognitive impairment. Compared with the normally aging SAM-resistant 1 (SAMR1), NPY-positive subpopulation of GABAergic neurons was reduced by 22–30% in the young SAMP8 hippocampus, leading to longer lasting epileptiform activity after high frequency stimulation. Reduction in the TH-activating type 2 deiodinase is suggested as a cause of this GABAergic impairment.

  4. Interferon gamma induces protective non-canonical signaling pathways in primary neurons

    Lauren A. O'Donnell, Kristen M. Henkins, Apurva Kulkarni, Christine M. Matullo, Siddharth Balachandran, Anil K. Pattisapu and Glenn F. Rall

    Article first published online: 31 AUG 2015 | DOI: 10.1111/jnc.13250

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    Interferon gamma (IFNγ) signaling varies depending upon cell type and the inflammatory milieu. In neurons, IFNγ activates extracellular regulated kinase-1/2 (Erk-1/2) low expression of the classical IFNγ signaling molecule Signal Transducers and Activators of Transcription-1 (STAT1). We propose that such alternative signaling pathways could protect against inflammation, and may be dictated by basal expression of intracellular signal transducers.

  5. Chandipura virus perturbs cholesterol homeostasis leading to neuronal apoptosis

    Sourish Ghosh, Sriparna Mukherjee and Anirban Basu

    Article first published online: 31 AUG 2015 | DOI: 10.1111/jnc.13208

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    Chandipura virus (CHPV) increases cholesterol import through low density lipid (LDL) receptor in neurons. Cholesterol in neurons are utilized to form the CHPV envelope. Excessive accumulation of cholesterol gets converted to 24(S)-hydroxycholesterol (24(S)-OHC) by cholesterol 24-hydroxylase enzyme (encoded by Cyp46a1 gene) that induces neuronal death through apoptosis. Therapeutics aimed against cholesterol homeostasis perturbation may be an effective anti-viral strategy.