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Journal of Neurochemistry

Cover image for Vol. 121 Issue 1

April 2012

Volume 121, Issue 1

Pages 1–180

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    1. You have free access to this content
      STOP-in the name of mood: microtubule-associated proteins in mood and cognition (pages 1–3)

      Patrick Schloss and Thorsten Lau

      Version of Record online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2011.07614.x

  2. REVIEW ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
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      Glial cells in (patho)physiology (pages 4–27)

      Vladimir Parpura, Michael T. Heneka, Vedrana Montana, Stéphane H. R. Oliet, Arne Schousboe, Philip G. Haydon, Randy F. Stout Jr, David C. Spray, Andreas Reichenbach, Thomas Pannicke, Milos Pekny, Marcela Pekna, Robert Zorec and Alexei Verkhratsky

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07664.x

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      Ketone bodies in epilepsy (pages 28–35)

      Melanie A. McNally and Adam L. Hartman

      Version of Record online: 7 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07670.x

  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    1. Signal Transduction & Synaptic Transmission

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      Kainate receptor-mediated depression of glutamatergic transmission involving protein kinase A in the lateral amygdala (pages 36–43)

      José Vicente Negrete-Díaz, Paloma Duque-Feria, Yuniesky Andrade-Talavera, Miriam Carrión, Gonzalo Flores and Antonio Rodríguez-Moreno

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07665.x

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      Presynaptic kainate receptor-mediated modulation of glutamate release in the lateral nucleus of the amygdala We wanted to determine the role of kainate receptors at thalamo-lateral amygdala synapses. The activation of presynaptic kainate receptors at these synapses inhibits glutamate release through a mechanism that involves the activation of protein kinase A. This action of kainate receptors could be involved in fear conditioning learning.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    1. Signal Transduction & Synaptic Transmission

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      The T-type voltage-gated calcium channel as a molecular target of the novel cognitive enhancer ST101: enhancement of long-term potentiation and CaMKII autophosphorylation in rat cortical slices (pages 44–53)

      Shigeki Moriguchi, Norifumi Shioda, Yui Yamamoto, Hideaki Tagashira and Kohji Fukunaga

      Version of Record online: 3 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07667.x

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      Novel Alzheimer disease therapeutics targeting for T-type voltage-gated Ca2+ channels We successfully developed novel cognitive enhancer, ST101. ST101 is under investigation of clinical trial phase 2 as Alzheimer disease therapeutics. We firstly discovered that ST101 stimulates Ca2+ current through T-type voltage-gated calcium channels, thereby promoting Ca2+/clmodulin-dependent protein kinase II (CaMKII) activity in the cortical and hippocampal neurons. Therefore, T-type voltage-gated calcium channels are unique and crucial targets for Alzheimer disease therapeutics.

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      Operation profile of zebrafish guanylate cyclase-activating protein 3 (pages 54–65)

      Ramona Fries, Alexander Scholten, Werner Säftel and Karl-Wilhelm Koch

      Version of Record online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2011.07643.x

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      The present study was performed to investigate the protein expression pattern of zGCAP3 and possible consequences of myristoylation. Probing larval and adult stages of the zebrafish retina indicated that zGCAP3 was first expressed in a nonmyristoylated form, but was myristoylated in the adult retina, which mainly helps to stabilize the protein. These results widen our view on protein myristoylation.

    3. Neuronal Plasticity & Behavior

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      Intraportal administration of DPP-IV inhibitor regulates insulin secretion and food intake mediated by the hepatic vagal afferent nerve in rats (pages 66–76)

      Kansuke Fujiwara, Koro Gotoh, Seiichi Chiba, Takayuki Masaki, Isao Katsuragi, Tetsuya Kakuma and Hironobu Yoshimatsu

      Version of Record online: 15 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07563.x

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      Neuronal pathways for glucose metabolism and feeding behavior Glucagon-like peptide-1 (GLP-1), rapidly degraded by dipeptidyl peptidase-IV (DPP-IV), affects glucose metabolism and feeding behavior. DPP-IV inhibitor-induced changes in portal but not systemic GLP-1 levels stimulate insulin secretion and suppress feeding, which are blocked by vagotomy, indicating a neuronal pathway that includes the hepatic vagal afferent nerve plays an important role in the pharmacological actions of DPP-IV inhibitor.

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      Hippocampal expression of myelin-associated inhibitors is induced with age-related cognitive decline and correlates with deficits of spatial learning and memory (pages 77–98)

      Heather D. VanGuilder, Georgina V. Bixler, William E. Sonntag and Willard M. Freeman

      Version of Record online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07671.x

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      Aged rats with impaired spatial learning and memory over-express myelin-associated inhibitors (MAIs). MAIs suppress neuronal plasticity, which is dysregulated with age-related cognitive decline. We demonstrate that expression of MAG, Nogo-A, OMgp and the NgR1 receptor is up-regulated in the hippocampus of aged rats with impaired spatial learning and memory, but not in their age-matched cognitively intact counterparts. Increased MAI signaling may underlie age-related deficits of hippocampal cognition by inhibiting structural and functional synaptic plasticity throughout the hippocampus.

    5. Molecular Basis of Disease

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      The deletion of STOP/MAP6 protein in mice triggers highly altered mood and impaired cognitive performances (pages 99–114)

      Vincent Fournet, Annie Schweitzer, Caroline Chevarin, Jean-Christophe Deloulme, Michel Hamon, Bruno Giros, Annie Andrieux and Marie-Pascale Martres

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07615.x

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      The deletion of MAP6/STOP protein triggers high imbalance in the serotonin and norepinephrine neurotransmissions between somas and terminals with functional consequences. STOP KO mice are depressed, less anxious and failed to perform in learning and memory tasks. Altogether, these data indicate that MAP6/STOP protein might have a crucial role in the serotonin and norepinephrine networks development.

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      Characterization of 1-(2-[18F]fluoro-3-pyridyl)-4-(2-isopropyl-1-oxo- isoindoline-5-yl)-5-methyl-1H-1,2,3-triazole, a PET ligand for imaging the metabotropic glutamate receptor type 1 in rat and monkey brains (pages 115–124)

      Masayuki Fujinaga, Jun Maeda, Joji Yui, Akiko Hatori, Tomoteru Yamasaki, Kazunori Kawamura, Katsushi Kumata, Yuichiro Yoshida, Yuji Nagai, Makoto Higuchi, Tetsuya Suhara, Toshimitsu Fukumura and Ming-Rong Zhang

      Version of Record online: 1 JUL 2011 | DOI: 10.1111/j.1471-4159.2011.07348.x

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      We developed [18F]FPIT as a PET ligand for imaging metabotropic glutamate receptor type 1 (mGluR1) in brain. [18F]FPIT exhibited in vitro and in vivo specific binding with mGluR1 in the rat and monkey brains, indicating its usefulness for imaging mGluR1 in the human brain.

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      Ammonia increases paracellular permeability of rat brain endothelial cells by a mechanism encompassing oxidative/nitrosative stress and activation of matrix metalloproteinases (pages 125–134)

      Marta Skowrońska, Magdalena Zielińska, Luiza Wójcik-Stanaszek, Joanna Ruszkiewicz, Dejan Milatovic, Michael Aschner and Jan Albrecht

      Version of Record online: 15 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07669.x

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      Changes in the blood–brain barrier (BBB) integrity due to degradation of tight junction proteins accompany hyperammonemia associated with acute liver failure, and increased activity of matrix metalloproteinases (MMPs) in blood has been suggested to be the causative factor. This study demonstrates that cerebral capillary endothelial cells forming the BBB can likewise be the source of BBB -damaging MMPs. Exposure of cultured cerebral capillary endothelial cells monolayers to ammonia increased paracellular passage of a 40 kDa protein (circles), which occurred subsequently to oxidative/nitrosative stress and increased MMP activity.

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      Val97Leu mutant presenilin-1 induces tau hyperphosphorylation and spatial memory deficit in mice and the underlying mechanisms (pages 135–145)

      Yue Wang, Zhe Cheng, Wei Qin and Jianping Jia

      Version of Record online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07489.x

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      A novel Val97Leu mutation of presenilin-1 impaired spatial memory and induced neuronal degeneration in mouse: We found a novel missense mutation of presenilin-1, Val97Leu, in members of a Chinese family that had early onset Alzheimer disease from a Chinese pedigree. The Val97Leu transgenic mice manifested a spatial memory deficit and neuronal degeneration, which was caused by GSK-3-dependent tau hyperphosphorylation. We concluded that a single point Val97Leu mutation of presenilin-1 is sufficient to cause deficit in brain memory.

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      Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage (pages 146–156)

      Kiichiro Okano, Akiko Maeda, Yu Chen, Vishal Chauhan, Johnny Tang, Grazyna Palczewska, Tsutomu Sakai, Hiroshi Tsuneoka, Krzysztof Palczewski and Tadao Maeda

      Version of Record online: 9 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07647.x

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      Rods are more susceptible than cones to light-induced damage: implications for human macular diseases We asked whether rods or cones are more susceptible to light-induced, all-trans-retinal-dependent damage and how any difference of susceptibility could affect the pathology of human macular diseases. Rods are more susceptible than cones to light-induced cell death; similar pathological changes were observed in patients with human macular disease. This finding can partially explain initial pathological events of human macular diseases and add to our understanding of these pathologies.

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      Synergistic inhibitory effect of nicotine plus oral contraceptive on mitochondrial complex-IV is mediated by estrogen receptor-β in female rats (pages 157–167)

      Ami P. Raval, Kunjan R. Dave, Isabel Saul, Gabriel J Gonzalez and Francisca Diaz

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07661.x

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      The severity of ischemic brain damage is greater in females simultaneously exposed to nicotine and oral contraceptives (NOC) than to nicotine alone. NOC inhibits mitochondrial estrogen receptor-beta signaling and mitochondrial functions in the brain. These findings distinguish the effects of nicotine from its combination with oral contraceptives in the female brain.

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      Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor (pages 168–179)

      Zeng-Jin Yang, Erin L. Carter, Kathleen K. Kibler, Herman Kwansa, Daina A. Crafa, Lee J. Martin, Richard J. Roman, David R. Harder and Raymond C. Koehler

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07666.x

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      Little is known about the role of 20-HETE in neonatal hypoxia-ischemia. Here, blockade of 20-HETE synthesis with HET0016 in newborn piglets after H-I had no significant effect on cerebral blood flow. However, it inhibited the PKC-dependent NMDA receptor and Na, K-ATPase phosphorylation, and improved Na, K-ATPase activity. Thus, 20-HETE can exert direct effects on proteins involved in neuronal excitotoxicity in immature brain.

  5. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    1. You have free access to this content
      CORRIGENDUM (page 180)

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2012.07663.x

      This article corrects:

      Inhibition of exocytosis or endocytosis blocks activity-dependent redistribution of synapsin

      Vol. 120, Issue 2, 248–258, Version of Record online: 2 DEC 2011

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