Journal of Neurochemistry

Cover image for Vol. 128 Issue 1

January 2014

Volume 128, Issue 1

Pages i–vii, 1–204

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. REVIEW
    6. ORIGINAL ARTICLES
    1. You have free access to this content
      Issue Cover (January 2014)

      Article first published online: 17 DEC 2013 | DOI: 10.1111/jnc.12530

      Thumbnail image of graphical abstract

      Front cover: Immunostaining for P0 (green) and neurofilament (red) of co-cultured dorsal root ganglion neurons and Schwann cells treated with the PSA mimetic nonyloxytryptamine after 21 DIV. DAPI staining (blue) was used to visualize cellular nuclei. Note that the number of P0/neurofilament double positive internodes on processes of dorsal root ganglion neurons is a measure for myelination.

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. REVIEW
    6. ORIGINAL ARTICLES
    1. You have free access to this content
      Issue Information (pages i–ii)

      Article first published online: 17 DEC 2013 | DOI: 10.1111/jnc.12531

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. REVIEW
    6. ORIGINAL ARTICLES
    1. You have free access to this content
  4. REVIEW

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. REVIEW
    6. ORIGINAL ARTICLES
    1. You have free access to this content
  5. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. REVIEW
    6. ORIGINAL ARTICLES
    1. Brain Development & Cell Differentiation

      Nonyloxytryptamine mimics polysialic acid and modulates neuronal and glial functions in cell culture (pages 88–100)

      Gabriele Loers, Vedangana Saini, Bibhudatta Mishra, Florentia Papastefanaki, David Lutz, Sidhartha Chaudhury, Daniel R. Ripoll, Anders Wallqvist, Sheraz Gul, Melitta Schachner and Gurcharan Kaur

      Article first published online: 23 SEP 2013 | DOI: 10.1111/jnc.12408

      Thumbnail image of graphical abstract

      Polysialic acid (PSA) plays important roles in nervous system development, as well as synaptic plasticity and regeneration in the adult. 5-Nonyloxytryptamine oxalate (5-NOT) mimics PSA and triggers PSA-mediated functions in neurons and glial cells. 5-NOT stimulates neuritogenesis, myelination and Schwann cell migration. This study sets the basis to develop a PSA-mediated therapy of acute and chronic nervous system diseases.

    2. Epigenetic activation of mouse ganglioside synthase genes: implications for neurogenesis (pages 101–110)

      Yi-Tzang Tsai and Robert K. Yu

      Article first published online: 23 OCT 2013 | DOI: 10.1111/jnc.12456

      Thumbnail image of graphical abstract

      Epigenetic regulation of two key regulatory glycosyltransferase (GT) genes, namely, GalNAcT and ST-II, has been presented in NECs. GalNAcT was also activated, as accompanied by induction of neuronal differentiation, in mouse NECs responding to exogenously added GM1, a product of the gene's encoding enzyme. Thus, ganglioside expression can be regulated by the epigenetic regulation of GT genes during neural development.

    3. Bioenergetics & Metabolism

      Modulation of intracellular ATP determines adenosine release and functional outcome in response to metabolic stress in rat hippocampal slices and cerebellar granule cells (pages 111–124)

      Stephanie zur Nedden, Alexander S. Doney and Bruno G. Frenguelli

      Article first published online: 11 SEP 2013 | DOI: 10.1111/jnc.12397

      Thumbnail image of graphical abstract

      The mammalian brain requires the purine salvage pathway to make ATP. However, at times of metabolic stress or traumatic injury, ATP metabolites are lost across the blood–brain barrier to the general circulation impairing both the resynthesis of ATP and compromising the ATP-derived reservoir of neuroprotective and anticonvulsant adenosine. By providing creatine, we can reduce ATP metabolism during metabolic stress, but at the expense of adenosine release, whilst d-ribose and adenine (RibAde) improve ATP levels and adenosine release, and protects neurones when given after metabolic stress. Creatine may thus have some neuroprophylactic value, whilst RibAde may promote metabolic and functional recovery after brain injury.

    4. In vivo quantification of neuro-glial metabolism and glial glutamate concentration using 1H-[13C] MRS at 14.1T (pages 125–139)

      Bernard Lanz, Lijing Xin, Philippe Millet and Rolf Gruetter

      Article first published online: 11 NOV 2013 | DOI: 10.1111/jnc.12479

      Thumbnail image of graphical abstract

      In this 13C-acetate labeling study, we propose a refined two-compartment analysis of brain energy metabolism based on 13C turnover curves of acetate, glutamate and glutamine measured with state of the art in vivo dynamic MRS at high magnetic field in rats, enabling a deeper understanding of the specific role of glial cells in brain oxidative metabolism. In addition, the robustness of the metabolic fluxes determination relative to MRS data quality was carefully studied.

    5. Molecular Basis of Disease

      Synaptodendritic recovery following HIV Tat exposure: Neurorestoration by phytoestrogens (pages 140–151)

      Sarah J. Bertrand, Charles F. Mactutus, Marina V. Aksenova, Tori D. Espensen-Sturges and Rosemarie M. Booze

      Article first published online: 26 AUG 2013 | DOI: 10.1111/jnc.12375

      Thumbnail image of graphical abstract

      The HIV-1 transactivating protein (Tat) is produced during viral latency in the brain. Treatment with either daidzein or liquiritigenin restored the loss of synaptic connectivity produced by HIV-1 Tat. This neurorestoration was mediated by estrogen receptors (ER). These results suggest that plant-derived phytoestrogens may promote recovery from HIV-1-induced synaptodendritic damage.

    6. Amphetamine stimulates movement through thalamocortical glutamate release (pages 152–161)

      Omar S. Mabrouk, Daniel Z. Semaan, Sarah Mikelman, Margaret E. Gnegy and Robert T. Kennedy

      Article first published online: 19 AUG 2013 | DOI: 10.1111/jnc.12378

      Thumbnail image of graphical abstract

      This study utilizes dual probe microdialysis sampling and comprehensive LC-MS analysis to determine the effects of amphetamine (1 mg/kg i.p.) on thalamocortical neurotransmission. Using pharmacological tools such as local thalamic tetrodotoxin (TTX) perfusion and glutamate antagonist at the cortical level, we demonstrate that thalamocortical glutamate (acting primarily through cortical AMPA receptors) is an essential component in amphetamine-induced hyperlocomotion.

    7. Dysregulation of leptin signaling in Alzheimer disease: evidence for neuronal leptin resistance (pages 162–172)

      David J. Bonda, Jeremy G. Stone, Sandy L. Torres, Sandra L. Siedlak, George Perry, Richard Kryscio, Gregory Jicha, Gemma Casadesus, Mark A. Smith, Xiongwei Zhu and Hyoung-gon Lee

      Article first published online: 21 AUG 2013 | DOI: 10.1111/jnc.12380

      Thumbnail image of graphical abstract

      In this study, increased leptin was found in CSF and hippocampus in Alzheimer disease indicating its physiological up-regulation, yet leptin receptor mRNA was decreased and leptin receptor protein was localized to neurofibrillary tangles, suggesting a discontinuity in the leptin signaling pathway. The lack of leptin signaling within degenerating neurons may represent a novel neuronal leptin resistance in Alzheimer disease.

    8. Detection of molecular alterations in methamphetamine-activated Fos-expressing neurons from a single rat dorsal striatum using fluorescence-activated cell sorting (FACS) (pages 173–185)

      Qing-Rong Liu, Francisco J. Rubio, Jennifer M. Bossert, Nathan J. Marchant, Sanya Fanous, Xingyu Hou, Yavin Shaham and Bruce T. Hope

      Article first published online: 21 AUG 2013 | DOI: 10.1111/jnc.12381

      Thumbnail image of graphical abstract

      Methamphetamine and other drugs activate a small proportion of all neurons in the brain. We here report an improved method to characterize molecular alterations induced selectively in activated neurons that express the neural activity marker Fos. We used FACS along with targeted PCR pre-amplification to assess acute methamphetamine-induced gene expression from as few as 5 Fos-expressing neurons from a single rat dorsal striatum. Methamphetamine induced 3–20-fold increases of immediate early genes (IEGs) in Fos-positive but not Fos-negative neurons. Targeted PCR pre-amplification makes it feasible to study unique molecular alterations in neurons activated by drugs or drug-associated cues in complex addiction models.

    9. Mechanism of cholesterol-assisted oligomeric channel formation by a short Alzheimer β-amyloid peptide (pages 186–195)

      Coralie Di Scala, Jean-Denis Troadec, Clément Lelièvre, Nicolas Garmy, Jacques Fantini and Henri Chahinian

      Article first published online: 28 AUG 2013 | DOI: 10.1111/jnc.12390

      Thumbnail image of graphical abstract

      Aβ22-35 peptide, which encompasses the cholesterol binding domain of Aβ, induces a specific increase of Ca2+ level in neural cells. Double mutations V24G/K28G and N27R/K28R modify cholesterol binding and abrogate channels formation. Molecular dynamic simulations suggest that cholesterol induces a tilted α-helical peptide topology facilitating the formation of annular octameric channels, as schematically shown in the graphic (with a hydrogen bond shown in green for two vicinal peptides). Overall, the data give insights into the role of cholesterol in amyloid channel formation and open up new therapeutic options for Alzheimer's disease.

    10. The neuroprotective activity of the amyloid precursor protein against traumatic brain injury is mediated via the heparin binding site in residues 96-110 (pages 196–204)

      Frances Corrigan, Emma Thornton, Laila C. Roisman, Anna V. Leonard, Robert Vink, Peter C. Blumbergs, Corinna van den Heuvel and Roberto Cappai

      Article first published online: 28 AUG 2013 | DOI: 10.1111/jnc.12391

      Thumbnail image of graphical abstract

      The product of α-secretase cleavage of the amyloid precursor protein, sAPPα is neuroprotective following traumatic brain injury (TBI). Of interest was whether this neuroprotective activity could be further delineated to a heparin binding region within sAPPα, corresponding to the region APP96-110 (see diagram demonstrating the domain structure of sAPPα). Indeed treatment with APP96-110 improved functional outcome following TBI, an effect that was not seen with a mutated version of the peptide that had reduced heparin binding affinity.

SEARCH

SEARCH BY CITATION