Journal of Neurochemistry

Cover image for Vol. 138 Issue 5

Edited By: Jörg Schulz

Impact Factor: 3.842

ISI Journal Citation Reports © Ranking: 2015: 71/256 (Neurosciences); 83/289 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. The oligodendrocyte-specific antibody ‘CC1’ binds Quaking 7

    Jenea M. Bin, Stephanie N. Harris and Timothy E. Kennedy

    Version of Record online: 24 AUG 2016 | DOI: 10.1111/jnc.13745

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    The monoclonal antibody anti-adenomatous polyposis coli (APC) clone CC1, is the antibody most commonly used to specifically label the cell bodies of mature oligodendrocytes. Despite being raised against APC, previous studies showed this antibody binds another unknown antigen. We show that the CC1 antibody binds Quaking (QKI) 7, an RNA-binding protein which is highly up-regulated in myelinating oligodendrocytes.

  2. Novel incretin analogues improve autophagy and protect from mitochondrial stress induced by rotenone in SH-SY5Y cells

    Jaishree Jalewa, Mohit Kumar Sharma and Christian Hölscher

    Version of Record online: 24 AUG 2016 | DOI: 10.1111/jnc.13736

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    GLP-1, GIP and dual incretin receptor agonists showed protective effects in SH-SY5Y cells treated with the stressor Rotenone. The novel GLP-1/GIP dual receptor agonist was superior and effective at a tenfold lower concentration compared to the other analogues. The drugs protected the cells from rotenone-induced impairment in cell growth and Akt activation, mitochondrial damage, impairments of autophagy and apoptotic cell signalling. See paper for details.

  3. You have free access to this content
    Targeting innate immunity for neurodegenerative disorders of the central nervous system (pages 653–693)

    Katrin I. Andreasson, Adam D. Bachstetter, Marco Colonna, Florent Ginhoux, Clive Holmes, Bruce Lamb, Gary Landreth, Daniel C. Lee, Donovan Low, Marina A. Lynch, Alon Monsonego, M. Kerry O'Banion, Milos Pekny, Till Puschmann, Niva Russek-Blum, Leslie A. Sandusky, Maj-Linda B. Selenica, Kazuyuki Takata, Jessica Teeling, Terrence Town and Linda J. Van Eldik

    Version of Record online: 24 AUG 2016 | DOI: 10.1111/jnc.13667

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    Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. This mini review series originated from the 4th Venusberg Meeting on Neuroinflammation held in Bonn, Germany, 7–9th May 2015, presenting updates on innate immunity in acute brain injury and chronic neurodegenerative disorders, such as traumatic brain injury and Alzheimer's disease, on the role of astrocytes and microglia, as well as technical developments that may help elucidate neuroinflammatory mechanisms and establish clinical relevance. In this meeting report, a brief overview on physiological and pathological microglia morphology is followed by a synopsis on PGE2 receptors, insights into the role of arginine metabolism and further relevant aspects of neuroinflammation in various clinical settings, and concluded by a presentation of technical challenges and solutions when working with microglia cultures. Microglial ontogeny and induced pluripotent stem cell-derived microglia, advances of TREM2 signaling, and the cytokine paradox in Alzheimer's disease are further contributions to this article.

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    Hippocampal PER1: a circadian sentinel controlling RSKy activity during memory formation (pages 650–652)

    Seung-Hee Yoo and Kristin Eckel-Mahan

    Version of Record online: 24 AUG 2016 | DOI: 10.1111/jnc.13727

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    Studies have demonstrated a pronounced dependence of memory formation on circadian time; however, the numerous mechanisms underlying this reliance are only beginning to be understood. While the 24-h cellular clock controls various aspects of hippocampal memory formation, its consolidation in particular (i.e., its conversion from short-term to long-term memory), appears to be heavily dependent on circadian activity in hippocampal neurons. Hippocampal memory consolidation requires phosphorylation of the cAMP Response Element-Binding protein, CREB, which upon phosphorylation promotes the transcription of genes necessary for long-term memory formation. Rhythmic cAMP/ERK-MAPK activity upstream of CREB is a necessary component. This Editorial highlights a study by Rawashdeh and coworkers, in which the authors establish the circadian clock gene Period1 (Per1) as a regulator of CREB phosphorylation in the mouse hippocampus, and thus reveal a functional link between circadian rhythms and learning efficiency.

    Read the highlighted article ‘Period1 gates the circadian modulation of memory-relevant signaling in mouse hippocampus by regulating the nuclear shuttling of the CREB kinase pP90RSK’ on page 731.

  5. Period1 gates the circadian modulation of memory-relevant signaling in mouse hippocampus by regulating the nuclear shuttling of the CREB kinase pP90RSK (pages 731–745)

    Oliver Rawashdeh, Antje Jilg, Erik Maronde, Jan Fahrenkrug and Jörg H. Stehle

    Version of Record online: 24 AUG 2016 | DOI: 10.1111/jnc.13689

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    We provide evidence that the circadian clock gene Period1 (Per1) regulates CREB phosphorylation in the mouse hippocampus, sculpturing time-of-day-dependent memory formation. This molecular mechanism constitutes the functional link between circadian rhythms and learning efficiency. In hippocampal neurons of wild-type mice, pP90RSK translocates into the nucleus upon stimulation with forskolin (left), whereas in Period1-knockout (Per1−/−) mice (right) the kinase is trapped at the nuclear periphery, unable to efficiently phosphorylate nuclear CREB. Consequently, the presence of PER1 in hippocampal neurons is a prerequisite for the time-of-day-dependent phosphorylation of CREB, as it regulates the shuttling of pP90RSK into the nucleus. Representative immunofluorescence images show a temporal difference in phosphorylated cAMP response element-binding protein (pCREB; green color) levels in all regions of the dorsal hippocampus between a wild-type C3H mouse (WT; left) and a Period1-knockout (Per1−/−; right) mouse. Images were taken 2 h after lights on, thus, when fluctuating levels of pCREB peak in WT mouse hippocampus. Insets show a representative hippocampal neuron, in response to activating cAMP signaling, stained for the neuronal marker NeuN (red), the nuclear marker DAPI (blue) and the activated CREB kinase pP90RSK (green). The image was taken 2 h after light onset (at the peak of the endogenous CREB phosphorylation that fluctuates with time of day). Magnification: 100X, inset 400X.

    Read the Editorial Highlight for this article on page 650.

    Cover image for this issue: doi: 10.1111/jnc.13332.