Journal of Neurochemistry

Cover image for Vol. 140 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. Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway

    Chong Xu, Xiaoxue Wang, Chenjian Gu, Hai Zhang, Ruijie Zhang, Xiaoqing Dong, Chunxiao Liu, Xiaoyu Hu, Xiang Ji, Shile Huang and Long Chen

    Version of Record online: 24 FEB 2017 | DOI: 10.1111/jnc.13966

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    We propose that celastrol, a plant-derived triterpene, ameliorates cadmium (Cd)-elicited neuronal apoptosis by preventing Cd from upregulating reactive oxygen species (ROS)-generating NOX2 and its regulatory proteins (p22phox, p40phox, p47phox, p67phox, and Rac1), thus suppressing ROS inactivation of PP5 and activation of JNK pathway. The findings highlight a beneficial role of celastrol in the prevention of Cd-induced oxidative stress and neurodegenerative diseases.

  2. P2Y12 receptors in primary microglia activate nuclear factor of activated T-cell signaling to induce C–C chemokine 3 expression

    Hidetoshi Tozaki-Saitoh, Hiroyuki Miyata, Tomohiro Yamashita, Katsuyuki Matsushita, Makoto Tsuda and Kazuhide Inoue

    Version of Record online: 24 FEB 2017 | DOI: 10.1111/jnc.13968

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    Extracellular nucleotides, like ADP, are recognized by P2Y12 receptors as a danger signal. Whether ADP/P2Y12 receptor signaling directly stimulates the production or release of inducible factors such as cytokines remains unclear. In this study, we demonstrate that ADP stimulates P2Y12 receptors, which leads to transient intracellular calcium increase and nuclear factor of activated T cell (NFAT) 1 activation. NFAT activation induces chemokine CCL3. These findings provide new concept that microglial P2Y12 receptors trigger an acute inflammatory response in microglia via NFAT activation leading to rapid chemokine induction, such as CCL3, after ADP stimulation.

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    The therapeutic potential of targeting chemokine signalling in the treatment of chronic pain

    Karli Montague and Marzia Malcangio

    Version of Record online: 24 FEB 2017 | DOI: 10.1111/jnc.13927

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    Chronic pain is poorly treated at present thus alternative therapies are essential. The critical role of chemokine-mediated communication between non-neuronal cells and neurons in the CNS and PNS in chronic pain has recently been appreciated. Here we discuss the therapeutic potential of targeting this chemokine-mediated communication, which is currently emerging as a promising strategy to treat chronic pain in patients.

  4. Involvement of chemokine CXCL11 in the development of morphine tolerance in rats with cancer-induced bone pain

    Genhua Guo, Yawen Peng, Bingrui Xiong, Daiqiang Liu, Huilian Bu, Xuebi Tian, Hui Yang, Zhen Wu, Fei Cao and Feng Gao

    Version of Record online: 24 FEB 2017 | DOI: 10.1111/jnc.13919

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    Chronic treatment with morphine induces the development of morphine antinociceptive tolerance. In this study, we provide novel evidence that spinal CXCL11, which could be released by both astrocytes and neurons, contributes to the development of morphine tolerance. This finding has significant therapeutic implications in prophylactically inhibiting morphine tolerance.

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    Nociception modulation by supraspinal group III metabotropic glutamate receptors

    Enza Palazzo, Ida Marabese, Livio Luongo, Francesca Guida, Vito de Novellis and Sabatino Maione

    Version of Record online: 22 FEB 2017 | DOI: 10.1111/jnc.13725

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    The modulatory actions of glutamate, the main excitatory neurotransmitter in the central nervous system (CNS), are exerted through the activation of metabotropic glutamate receptors (mGluRs). Novel ligands that are selective for group III mGluR subtypes have recently been developed. These compounds, which mainly target allosteric sites and act as positive or negative allosteric modulators (PAMs or NAMs) of glutamate transmission, contribute to the understanding of the functional roles of group III mGluRs in a number of pathological conditions, such as epilepsy, anxiety, neurodegenerative diseases, and chronic pain. This review summarizes recent studies on group III mGluRs in animal models of chronic pain which evidenced an opposite modulation of mGluR7 and mGluR8 on pain responses and their capability to affect pain responses only in pathological states.