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. Proteomics-level analysis of myelin formation and regeneration in a mouse model for Vanishing White Matter disease

    Irit Gat-Viks, Tamar Geiger, Mali Barbi, Gali Raini and Orna Elroy-Stein

    Accepted manuscript online: 28 APR 2015 09:55AM EST | DOI: 10.1111/jnc.13142

  2. Activation of PI3Kγ/Akt pathway mediates bone cancer pain in rats

    Xuehai Guan, Qiaochu Fu, Bingrui Xiong, Zhenpeng Song, Bin Shu, Huilian Bu, Bing Xu, Anne Manyande, Fei Cao and Yuke Tian

    Accepted manuscript online: 28 APR 2015 02:50AM EST | DOI: 10.1111/jnc.13139

  3. Identification of precursor microRNAs within distal axons of sensory neuron

    Hak Hee Kim, Paul Kim, Monichan Phay and Soonmoon Yoo

    Accepted manuscript online: 28 APR 2015 02:49AM EST | DOI: 10.1111/jnc.13140

  4. Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury

    Yang Gao, Siyi Xu, Zhenwen Cui, Mingkun Zhang, Yingying Lin, Lei Cai, Zhugang Wang, Xingguang Luo, Yan Zheng, Yong Wang, Qizhong Luo, Jiyao Jiang, Joseph H. Neale and Chunlong Zhong

    Article first published online: 28 APR 2015 | DOI: 10.1111/jnc.13123

    Thumbnail image of graphical abstract

    The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) suppresses glutamate transmission through selective activation of pre-synaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3) after traumatic brain injury (TBI). However, synaptically released NAAG is hydrolyzed to form N-acetylaspartate and glutamate mainly by Glutamate carboxypeptidase II (GCPII), losing neuroprotective effect. In this study, we found that knock out of the GCPII gene is not embryonic lethal and affords histopathological protection with improved long-term behavioral outcomes after TBI.

  5. The regulation of p53 up-regulated modulator of apoptosis by JNK/c-Jun pathway in β-amyloid-induced neuron death

    Rumana Akhter, Priyankar Sanphui, Hrishita Das, Pampa Saha and Subhas Chandra Biswas

    Article first published online: 28 APR 2015 | DOI: 10.1111/jnc.13128

    Thumbnail image of graphical abstract

    JNK/c-Jun pathway is shown to be activated in neurons of the Alzheimer's disease (AD) brain and plays a vital role in neuron death in AD models. However, downstream targets of c-Jun in this disease have not been thoroughly elucidated. Our study shows that two important pro-apoptotic proteins, Bim (Bcl-2 interacting mediator of cell death) and Puma (p53 up-regulated modulator of apoptosis) are targets of c-Jun in Aβ-treated neurons. We demonstrate that the JNK/c-jun pathway is activated, in cultures of cortical neurons following treatment with oligomeric Aβ and in AD transgenic mice, and that inhibition of this pathway by selective inhibitor blocks induction of Puma by Aβ. We have also observed functional co-operation of both JNK and p53 pathway in regulation of Puma under Aβ toxicity. Most importantly, we identified a novel AP1-binding site on rat puma gene which is necessary for direct binding of c-Jun with Puma promoter. Thus, our results suggest that both Bim and Puma are target of c-Jun and elucidate the intricate regulation of Puma expression by JNK/c-Jun and p53 pathways in neurons upon Aβ toxicity.