Journal of Neurochemistry

Cover image for Vol. 135 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 microglial TLR3 promotes neuronal survival against cerebral ischemia

    Si-Yeon Jeong, Raok Jeon, Yoon Kyung Choi, Joo Eun Jung, Anna Liang, Changhong Xing, Xiaoying Wang, Eng H. Lo and Yun Seon Song

    Accepted manuscript online: 25 NOV 2015 06:28AM EST | DOI: 10.1111/jnc.13441

  2. Expression of class II HDACs in two mouse models of temporal lobe epilepsy

    Rohan Jagirdar, Meinrad Drexel, Anneliese Bukovac, Ramon O. Tasan and Günther Sperk

    Accepted manuscript online: 25 NOV 2015 06:24AM EST | DOI: 10.1111/jnc.13440

  3. The dipeptidyl peptidase IV inhibitor vildagliptin suppresses development of neuropathy in diabetic rodents: Effects on peripheral sensory nerve function, structure and molecular changes

    Kentaro Tsuboi, Hiroki Mizukami, Wataru Inaba, Masayuki Baba and Soroku Yagihashi

    Accepted manuscript online: 25 NOV 2015 06:21AM EST | DOI: 10.1111/jnc.13439

  4. Remarkable impairment of Wnt/β-catenin signaling in the brains of the mice infected with scrapie agents

    Jing Sun, Hui Wang, Li-Na Chen, Jing Wang, Yan Lv, Xiao-Dong Yang, Bao-Yun Zhang, Chan Tian, Qi Shi and Xiao-Ping Dong

    Article first published online: 25 NOV 2015 | DOI: 10.1111/jnc.13416

    Thumbnail image of graphical abstract

    Schematic for the impairment of canonical Wnt signaling during prion infection. The left and right parts represent the normal and prion-infected situations, respectively. Prion infection or PrPSc accumulation triggers the over-expression of Dickkopf WNT signaling pathway inhibitor 1 (DKK-1) and the enhancement of glycogen synthase kinase 3β (GSK-3β) activity, which subsequently promotes the phosphorylation and degradation of β-catenin. As a result, the impairment of β-catenin signaling leads to the down-regulation of Wnt target genes.

  5. No improvement of neuronal metabolism in the reperfusion phase with melatonin treatment after hypoxic-ischemic brain injury in the neonatal rat

    Hester R. Berger, Tora Sund Morken, Riyas Vettukattil, Ann-Mari Brubakk, Ursula Sonnewald and Marius Widerøe

    Article first published online: 24 NOV 2015 | DOI: 10.1111/jnc.13420

    Thumbnail image of graphical abstract

    Neuronal and astrocytic metabolism was examined by 13C and 1H NMR spectroscopy in the early reperfusion phase after unilateral hypoxic-ischemic brain injury and melatonin treatment in neonatal rats. One hour after hypoxia-ischemia astrocytic mitochondrial metabolism had recovered and glycolysis was normalized, whereas mitochondrial metabolism in neurons was impaired. Melatonin treatment did not show a protective effect on neuronal metabolism.