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Journal of Neurochemistry

Cover image for Vol. 121 Issue 2

April 2012

Volume 121, Issue 2

Pages 181–326


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    4. ERRATUM
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      Matrix metalloproteinase-9 and non-amyloidogenic pathway of amyloid precursor protein processing (pages 181–183)

      Mikhail A. Filippov and Alexander Dityatev

      Version of Record online: 4 APR 2012 | DOI: 10.1111/j.1471-4159.2011.07641.x


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    1. Signal Transduction & Synaptic Transmission

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      Synaptic vesicles are capable of synthesizing the VGLUT substrate glutamate from α-ketoglutarate for vesicular loading (pages 184–196)

      Kouji Takeda, Atsuhiko Ishida, Kento Takahashi and Tetsufumi Ueda

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07684.x

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      Synaptic vesicle loading of glutamate is the first step in glutamate synaptic transmission. We provide evidence that the VGLUT substrate glutamate is locally synthesized on the surface of vesicles from α-ketoglutarate and aspartate by aspartate aminotransferase, and taken up into vesicles, indicating high efficiency in glutamate transmission. We have also found that 2,3-pyrazinedicarboxylate inhibits this synthetic enzyme. Finding this inhibitor has important implications for defining the role of vesicle-bound aspartate aminotransferase in glutamate transmission.

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      Vol. 122, Issue 2, 482, Version of Record online: 1 JUN 2012

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      Sertraline inhibits pre-synaptic Na+ channel-mediated responses in hippocampus-isolated nerve endings (pages 197–205)

      Blanca I. Aldana and María Sitges

      Version of Record online: 20 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07674.x

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      Na+ channels controlling neurotransmitter release, a novel aspect in sertraline mechanism of action. Sertraline is known as a selective 5-HT transporter (SERT) inhibitor. Here, we found that in addition to its 5-HT reuptake blocking action, that selectively increases 5-HT under baseline conditions, sertraline inhibits 5-HT, Glu and GABA release triggered by the Na+ channel opener veratridine in hippocampal isolated nerve endings. These findings demonstrate that the antidepressant sertraline is an effective inhibitor of cerebral pre-synaptic Na+ channels.

    3. Neuroinflammation & Neuroimmunology

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      The vincamine derivative vindeburnol provides benefit in a mouse model of multiple sclerosis: effects on the Locus coeruleus (pages 206–216)

      Paul E. Polak, Sergey Kalinin, David Braun, Anthony Sharp, Shao X. Lin and Douglas L. Feinstein

      Version of Record online: 17 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07673.x

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      Protecting the Locus coeruleusFindings that noradrenergic neurons in the Locus coeruleus (LC) of MS patients are damaged suggest that drugs which increase LC neuronal survival or function could be of value. Vindeburnol, a vincamine derivative previously shown to increase LC function, reduced clinical signs, lesions, and inflammation in EAE mice; associated with reduced LC damage and higher noradrenaline levels. These findings identify the LC as a potential target for MS treatment.

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      Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration (pages 217–227)

      Keiko Ohsawa, Tomomi Sanagi, Yasuko Nakamura, Eri Suzuki, Kazuhide Inoue and Shinichi Kohsaka

      Version of Record online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07693.x

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      Process extension and migration of microglia towards injured sites in the brain are triggered by the stimulation of the purinergic receptor P2Y12 with extracellular ATP. Our results indicate that adenosine, a phosphohydrolytic derivative of ATP, promoted P2Y12-mediated process extension and migration through the adenosine A3 receptor. These findings suggest that A3 signaling cooperates with P2Y12 to regulate the chemotactic motion of microglia in response to neuronal damage.

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      Nucleotides released from Aβ1–42-treated microglial cells increase cell migration and Aβ1–42 uptake through P2Y2 receptor activation (pages 228–238)

      Hye Jung Kim, Deepa Ajit, Troy S. Peterson, Yanfang Wang, Jean M. Camden, W. Gibson Wood, Grace Y. Sun, Laurie Erb, Michael Petris and Gary A. Weisman

      Version of Record online: 14 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07700.x

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      Nucleotides released from apoptotic cells in the brain activate microglia to promote clearance of cell debris. This study demonstrates the role of P2Y2 receptors for extracellular nucleotides in the phagocytosis of Aβ in mouse microglial cells. Results indicate that nucleotides cause a significant increase in Aβ uptake in wildtype microglial cells, but not in cells from P2Y2 receptor knockout mice, suggesting that the P2Y2 receptor is a novel therapeutic target in AD.

    6. Neuronal Plasticity & Behavior

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      Enhanced neuronal plasticity and elevated endogenous sAPPα levels in mice over-expressing MMP9 (pages 239–251)

      Apostolia Fragkouli, Costas Papatheodoropoulos, Spiros Georgopoulos, Antonios Stamatakis, Fotini Stylianopoulou, Effie C. Tsilibary and Athina K. Tzinia

      Version of Record online: 9 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07637.x

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      Beneficial effects of MMP9 in the brain To investigate MMP9 effect on neuronal plasticity in vivo, we have generated a transgenic mouse line over-expressing MMP9 in brain neurons. Over-expression of MMP9 in the brain results to enhanced synaptic plasticity, improved cognitive abilities and increased secretion of the neurotrophic sAPPα. APP may be a physiological target of MMP9 and sAPPα might participate in MMP9 plasticity-enhancing effects in vivo.

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      Sources contributing to the average extracellular concentration of dopamine in the nucleus accumbens (pages 252–262)

      Catarina A. Owesson-White, Mitchell F. Roitman, Leslie A. Sombers, Anna M. Belle, Richard B. Keithley, Jessica L. Peele, Regina M. Carelli and R. Mark Wightman

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07677.x

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      Extracellular dopamine concentration in the nucleus accumbens. In this work, we find that transient increases in extracellular dopamine due to phasic firing of dopaminergic neurons contribute to an average extracellular concentration that is similar to the basal level established by low flow-rate microdialysis. Contributions from tonic firing were below detection limit and thus relatively small. That tonic firing contributes negligible amounts to the basal level lends further support to the idea that dopamine transients are required to activate dopamine receptors in awake and behaving rats.

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      Resistance to trophic neurite outgrowth of sensory neurons exposed to insulin (pages 263–276)

      Bhagat Singh, Yongqin Xu, Todd McLaughlin, Vandana Singh, Jose A. Martinez, Anand Krishnan and Douglas W. Zochodne

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07681.x

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      Neurons develop insulin resistance: Bhagat et al. examined whether sensory neurons, those primarily targeted by diabetic neuropathy, develop resistance to the trophic properties of insulin. The work shows that primary adult sensory neurons, in response to high dose or prolonged insulin, undergo loss of their neurite outgrowth capacity to insulin through down-regulation of insulin receptors and up-regulation of GSK-3β. Insulin resistance may contribute toward diabetic polyneuropathy.

    9. Molecular Basis of Disease

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      γ-Secretase modulators do not induce Aβ-rebound and accumulation of β-C-terminal fragment (pages 277–286)

      Ting Li, Yunhong Huang, Shiyi Jin, Liang Ye, Na Rong, Xiujuan Yang, Yu Ding, Ziqiang Cheng, Jinqiang Zhang, Zehong Wan, David C. Harrison, Ishrut Hussain, Adrian Hall, Daniel Hong Seng Lee, Lit-Fui Lau and Yasuji Matsuoka

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2011.07560.x

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      γ-secretase modulators avoid paradoxical Aβ rebound and accumulation of β-C-terminal fragment caused by γ-secretase inhibitors. A γ-secretase inhibitor, LY-450139, designed to slow cognitive decline in Alzheimer’s patients ended up doing the opposite in a phase III trial. LY-450139 is known to cause paradoxical Aβ rebound, the significance of which in the adverse effects remains to be determined. γ-Secretase modulators can reduce Aβ 40 and 42 without triggering Aβ rebound and β-CTF accumulation. They might be a better alternative in treating Alzheimer’s disease.

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      Microglial neurotransmitter receptors trigger superoxide production in microglia; consequences for microglial–neuronal interactions (pages 287–301)

      Emma L. Mead, Angelina Mosley, Simon Eaton, Lucianne Dobson, Simon J. Heales and Jennifer M. Pocock

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07659.x

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      Microglial neurotransmitter receptors couple to intracellular superoxide generation Microglia express a wide range of neurotransmitter receptors but little is known about the signalling cascades activated when these receptors are stimulated. Stimulation of glutamate, GABA or ATP receptors triggered intracellular superoxide production in microglia. Theese findings will help to target therapies to known receptors on microglia to modulate the wayward microglial responses detected in a wide range of neurodegenerative diseases.

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      Cocaine decreases expression of neurogranin via alterations in thyroid receptor/retinoid X receptor signaling (pages 302–313)

      Jane Kovalevich, Gladys Corley, William Yen, Jae Kim, Scott M. Rawls and Dianne Langford

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07678.x

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      Neurogranin (Ng) is expressed by neurons and regulates synaptic plasticity. We show that cocaine decreases Ng expression via alterations in 9-cis-RA availability and TR/RXR-g signaling. Transcriptional activation of Ng requires both thyroid hormone (T3) and 9-cis-RA; thus, levels of either T3 or RA could be limiting factors in Ng expression. While T3 levels did not change, CYP26A1, the enzyme that degrades neuronal RA, was significantly up-regulated by cocaine. Results from this study provide the first evidence for a direct effect of cocaine on TR/RXR signaling, RA metabolism, and transcriptional regulation of Ng, a gene essential for adult neuroplasticity.

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      Plasma desmoplakin I biomarker of vascular recurrence after ischemic stroke (pages 314–325)

      Antonio J. López-Farré, José J. Zamorano-León, Antonio Segura, Petra J. Mateos-Cáceres, Javier Modrego, Pablo Rodríguez-Sierra, Laura Calatrava, Juan Tamargo and Carlos Macaya

      Version of Record online: 13 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07683.x

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      Plasma desmoplakin I and vascular post-stroke recurrence The present study used proteomics to identify novel plasma biomarkers associated with vascular recurrence in post-stroke ischemic patients. High plasma desmoplakin I levels in patients taking statins in the three first months after the first ischemic stroke were associated with protection against a new vascular event in one year of follow-up. This result suggests that plasma desmoplakin I may serve as a biomarker for good response to statins in post-stroke ischemic patients.


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    4. ERRATUM
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      Erratum (page 326)

      Version of Record online: 17 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07687.x

      This article corrects:

      Pathogenic implications of iron accumulation in multiple sclerosis

      Vol. 120, Issue 1, 7–25, Version of Record online: 11 NOV 2011