Journal of Neurochemistry

Cover image for Vol. 133 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

  1. Tyrosine Hydroxylase Positive Perisomatic Rings are Formed around Various Amacrine Cell Types in the Mammalian Retina

    Gábor Debertin, Orsolya Kántor, Tamás Kovács-Öller, Lajos Balogh, Edina Szabó-Meleg, József Orbán, Miklós Nyitrai and Béla Völgyi

    Accepted manuscript online: 4 MAY 2015 09:04AM EST | DOI: 10.1111/jnc.13144

  2. p35 and Rac1 underlie the neuroprotection and cognitive improvement induced by CDK5 silencing

    Rafael Andres Posada-Duque, Alejandro López-Tobón, Diego Piedrahita, Christian González-Billault and Gloria Patricia Cardona-Gomez

    Article first published online: 4 MAY 2015 | DOI: 10.1111/jnc.13127

    Thumbnail image of graphical abstract

    CDK5 plays an important role in neurotransmission in the normal function of the adult brain, and dysregulation can lead to Tau hyperphosphorylation and cognitive impairment. Our findings suggest that p35/Rac1 signaling is critical in the CDK5 shRNAmiR-induced neuroprotection against glutamate neurotoxicity and is also correlated with the recovery of cognitive function in 3xTg-AD mice. CDK5 shRNAmiR blocks calpain activation, and the cleavage of p35 to p25 produced by glutamate, which generates neuroprotection in a p35 up-regulation dependent mode and its down-stream control of Rho GTPases, such as Rac1 and RhoA.

  3. Nidogen-1 is a common target of microRNAs MiR-192/215 in the pathogenesis of Hirschsprung's disease

    Dongmei Zhu, Hua Xie, Hongxing Li, Peng Cai, Hairong Zhu, Chao Xu, Pingfa Chen, Ankur Sharan, Yankai Xia and Weibing Tang

    Article first published online: 4 MAY 2015 | DOI: 10.1111/jnc.13118

    Thumbnail image of graphical abstract

    We proposed the following cascade for the proposed mechanism of miR-192/215 in the pathogenesis of Hirschsprung disease (HSCR) by targeting Nidogen 1 (NID1). Aberrant expression of miR-192/215 inhibits cell migration and cell proliferation via NID1. We think the miR-192/miR-215/NID1 signaling pathway may play an important role in the pathogenesis of HSCR.

  4. Postnatal ethanol exposure alters levels of 2-arachidonylglycerol-metabolizing enzymes and pharmacological inhibition of monoacylglycerol lipase does not cause neurodegeneration in neonatal mice

    Shivakumar Subbanna, Delphine Psychoyos, Shan Xie and Balapal S. Basavarajappa

    Article first published online: 30 APR 2015 | DOI: 10.1111/jnc.13120

    Thumbnail image of graphical abstract

    The consumption of ethanol by pregnant women may cause neurological abnormalities, affecting learning and memory processes in children, and are collectively described as fetal alcohol spectrum disorders (FASDs). In our study, ethanol treatment of postnatal day 7 (P7) mice significantly enhanced the levels of the developmentally relevant endocannabinoids anandamide (AEA) but not 2-arachidonylglycerol (2-AG), and induced widespread neurodegeneration, yet the reason for the lack of effects of ethanol on the 2-AG level is unknown. Here, the ethanol treatment of P7 mice causes the specific up-regulation of AEA-CB1R signaling over the 2-AG-CB1R pathway by the specific reorganization of the enzymes that synthesize (DAGL-α/β) and degrade (MAGL) 2-AG. This study demonstrates the neuro-regulatory role of 2-AG metabolizing enzymes in ethanol-induced neurodegeneration in neonatal mice.

  5. Input-specific regulation of hippocampal circuit maturation by non-muscle Myosin IIB

    Emin D. Ozkan, Massimiliano Aceti, Thomas K. Creson, Camilo S. Rojas, Cristopher Hubbs, Megan N. McGuire, Priyanka P. Kakad, Courtney A. Miller and Gavin Rumbaugh

    Accepted manuscript online: 30 APR 2015 10:17AM EST | DOI: 10.1111/jnc.13146

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