Journal of Neurochemistry

Cover image for Vol. 139 Issue 1

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. Calpain inhibition reduces structural and functional impairment of retinal ganglion cells in experimental optic neuritis

    Amena W. Smith, Baerbel Rohrer, Lee Wheless, Supriti Samantaray, Swapan K. Ray, Jun Inoue, Mitsuyoshi Azuma and Naren L. Banik

    Version of Record online: 27 SEP 2016 | DOI: 10.1111/jnc.13770

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    As in multiple sclerosis (MS) patients, optic neuritis (ON) and early, primarily monocular loss in spatial acuity is observed in a rodent model (EAE, experimental autoimmune encephalomyelitis). Daily oral treatment with the calpain inhibitor SNJ 1945 preserves visual acuity and preserves retinal ganglion cells (Brn3a, brain-specific homeobox/POU domain protein 3A) and their axons (MOSP, myelin oligodendrocyte-specific protein). Calpain inhibition may represent a candidate therapy for the preservation of vision in ON.

  2. Tyrosine kinase inhibition reverses TDP-43 effects on synaptic protein expression, astrocytic function and amino acid dis-homeostasis

    Lanier Heyburn, Michaeline L. Hebron, Jacqueline Smith, Charisse Winston, John Bechara, Zhaoxia Li, Irina Lonskaya, Mark P. Burns, Brent T. Harris and Charbel E.-H. Moussa

    Version of Record online: 27 SEP 2016 | DOI: 10.1111/jnc.13763

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    To analyze molecular mechanism underlying the trans-activating response of DNA/RNA-binding protein (TDP)-43 pathology, transgenic mice over-expressing human TDP-43 were analyzed for their glutamate metabolism and synaptic function. Over-expression of TDP-43 leads to reduction of presynaptic protein expression, including synaptotagmin and synapsin and decreased astrocytic activity. Furthermore, it increases levels of glutamate and GABA and reduces levels of glutamine and aspartate, suggesting impairment of the neuronal-astrocytic glutamate–glutamine cycle. TDP-43 also decreases tricarboxylic acid metabolism and induces oxidative stress via lactate accumulation. Treatment of TDP-43 transgenic mice with tyrosine kinase inhibitors (TKIs) leads to an increase in astrocyte function, restoration of neurotransmitter homeostasis, reduction of oxidative stress and a decrease in VEGF levels. It is hypothesized that TKIs reduce TDP-43 levels in neurons and increase presynaptic protein levels, leading to restoration of glutamate detoxification via the glutamate–glutamine cycle in activated astrocytes.

  3. Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury

    Louis J. Sparvero, Andrew A. Amoscato, Arthur B. Fink, Tamil Anthonymuthu, Lee Ann New, Patrick M. Kochanek, Simon Watkins, Valerian E. Kagan and Hulya Bayır

    Version of Record online: 26 SEP 2016 | DOI: 10.1111/jnc.13840

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    Traumatic brain injury (TBI) leads to changes in ion fluxes and alterations in mitochondrial function. Mitochondrial signaling strongly depends on cardiolipin (CL), which is selectively oxidized and presents itself as a target for redox therapy following TBI. We describe a mass spectrometric lipid imaging study that reports regio-specific changes in rat brain CL in a controlled cortical impact (CCI) model of traumatic brain injury (TBI). While MALDI-MS imaging revealed that TBI caused decreases in CL in the contusional area 3 h after injury, it also revealed decreases extending well beyond the area of impact into histologically normal tissue in the hippocampus and thalamic regions. The more unsaturated CL species were most susceptible to loss.

  4. Cannabinoid receptor interacting protein suppresses agonist-driven CB1 receptor internalization and regulates receptor replenishment in an agonist-biased manner

    Lawrence C. Blume, Sandra Leone-Kabler, Deborah J. Luessen, Glen S. Marrs, Erica Lyons, Caroline E. Bass, Rong Chen, Dana E. Selley and Allyn C. Howlett

    Version of Record online: 26 SEP 2016 | DOI: 10.1111/jnc.13767

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    The CB1R-interacting protein CRIP1a functions to differentially modulate agonist-promoted versus non-agonist-mediated CB1R internalization and cell surface equilibrium. Association of CRIP1a with the CB1R precludes agonist-driven internalization via a mechanism involving β-arrestin, clathrin and dynamin. CRIP1a also functions to fine-tune CB1R cell surface levels through delivery of newly synthesized CB1R receptors to the plasma membrane.

  5. Donepezil promotes differentiation of neural stem cells into mature oligodendrocytes at the expense of astrogenesis

    Osamu Imamura, Masaaki Arai, Minori Dateki and Kunio Takishima

    Accepted manuscript online: 24 SEP 2016 11:30AM EST | DOI: 10.1111/jnc.13856