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. 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.

  2. 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.

  3. 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.

  4. 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.

  5. Nicotine administration in the wake-promoting basal forebrain attenuates sleep-promoting effects of alcohol

    Rishi Sharma, Shafi Lodhi, Pradeep Sahota and Mahesh M. Thakkar

    Article first published online: 31 AUG 2015 | DOI: 10.1111/jnc.13219

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    Alcohol and nicotine are highly co-abused. The underlying mechanism is unclear. One reason why people use nicotine, a stimulant, with alcohol is to enhance recreational/pleasurable sensations while suppressing alcohol's aversive effects such as sleepiness. We have previously observed that nicotine acts via wake-promoting basal forebrain to increase alcohol consumption and activate nucleus accumbens, the pleasure center. Here, we demonstrate that nicotine acts via the basal forebrain to suppress sleep-promoting effects of alcohol further implicating the basal forebrain as a key substrate in nicotine alcohol co-use.

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