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Journal of Neurochemistry

Cover image for Vol. 122 Issue 5

September 2012

Volume 122, Issue 5

Pages 869–1093

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATIONS
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. ERRATUM
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  2. REVIEW

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATIONS
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. ERRATUM
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      Histamine in brain development (pages 872–882)

      Anayansi Molina-Hernández, Néstor Fabián Díaz and José-Antonio Arias-Montaño

      Article first published online: 3 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07863.x

  3. SHORT COMMUNICATIONS

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATIONS
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. ERRATUM
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      Cross-seeding effects of amyloid β-protein and α-synuclein (pages 883–890)

      Kenjiro Ono, Ryoichi Takahashi, Tokuhei Ikeda and Masahito Yamada

      Article first published online: 23 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07847.x

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      Previous studies have suggested that interactions between amyloid β-protein (Aβ) and α-synuclein (αS) are involved in the pathogenesis of Alzheimer’s disease (AD) and Lewy body diseases (LBD). Fibrils and oligomers of Aβ and αS acted as seeds, and affected the aggregations with each other. These may contribute to our understanding of the molecular mechanisms of interactions between AD and LBD.

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      Presynaptic kainate receptor-mediated facilitation of glutamate release involves Ca2+–calmodulin at mossy fiber–CA3 synapses (pages 891–899)

      Yuniesky Andrade-Talavera, Paloma Duque-Feria, José Vicente Negrete-Díaz, Talvinder S. Sihra, Gonzalo Flores and Antonio Rodríguez-Moreno

      Article first published online: 23 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07844.x

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      Ca 2+ -calmodulin involvement in presynaptic kainate receptors modulation of glutamate release in the hippocampusWe wanted to determine the mechanism by which kainate receptors could activate AC at MF–CA3 synapses of the hippocampus. We have discovered that an increase in Ca2+ levels in the cytosol of MF terminals operates through the formation of Ca2+–calmodulin complexes to activate AC. This signal coupling is also necessary for LTP induction. The action of kainate receptors mediated through Ca-calmodulin/AC signaling could therefore be involved in learning and memory processes.

  4. ORIGINAL ARTICLES

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

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      Expression of GABAρ receptors in the neostriatum: localization in aspiny, medium spiny neurons and GFAP-positive cells (pages 900–910)

      Abraham Rosas-Arellano, Arturo I. Machuca-Parra, Daniel Reyes-Haro, Ricardo Miledi and Ataúlfo Martínez-Torres

      Article first published online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07621.x

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      GABAρ receptors in neurons and astrocytes of striatum GABA transmission plays a central role in the interneurons of the striatum. We aimed to investigate whether GABAρ receptors, which are bicuculline-resistant and do not desensitize are expressed in this area. We found that GABAρ are present in calretinin neurons and astrocyes, and although the receptors are sensitive to TPMPA, they most likely form heteromeric complexes with other GABA subunits.

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      ERK1/2, p38, and JNK regulate the expression and the activity of the three isoforms of the Na+/Ca2+exchanger, NCX1, NCX2, and NCX3, in neuronal PC12 cells (pages 911–922)

      Rossana Sirabella, Agnese Secondo, Anna Pannaccione, Pasquale Molinaro, Luigi Formisano, Natascia Guida, Gianfranco Di Renzo, Lucio Annunziato and Mauro Cataldi

      Article first published online: 11 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07838.x

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      In central nervous system the sodium-calcium exchanger (NCX) is involved in the control of MAPK-dependent processes like learning, memory, and cell survival after hypoxia. Here we show that in neuronal PC12 cells MAPKs differentially control the three NCX isoforms and, consequently, total NCX activity. These findings suggest that NCX could be involved in mediating some of MAPK effects in neurons.

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      Synaptic relationship between somatostatin- and neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complex of rats (pages 923–933)

      Xiao-Yan Wei, Yu Zhao, Margaret T. T. Wong-Riley, Gong Ju and Ying-Ying Liu

      Article first published online: 3 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07862.x

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      Somatostatin-immunoreactive terminals synapse with neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complexUnderstanding synaptic relationship of SST/NK1R-ir neurons in the pre-BötC is essential in providing cellular and structural bases for their physiological significance. We found that SST-ir terminals were glutamatergic or GABAergic, and made asymmetric or symmetric synapses with NK1R-ir neurons. We propose a SST-mediated excitatory–inhibitory synaptic transmission onto NK1R-ir neurons that synchronizes their activities in contribution to respiratory rhythmogenesis and control.

    4. Bioenergetics & Metabolism

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      Inhibition of NMDA-type glutamate receptors induces arousal from torpor in hibernating arctic ground squirrels (Urocitellus parryii) (pages 934–940)

      Tulasi R. Jinka, Brian T. Rasley and Kelly L. Drew

      Article first published online: 11 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07832.x

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      Signal to arouse from hibernation Hibernation is a strategy to conserve energy and overcome extreme weather conditions and scarcity in resources. The hibernation season consists of prolonged bouts of torpor that are interrupted by brief interbout arousals. Energetically expensive interbout arousals serve many functions, but the mechanism that induces spontaneous interbout arousal is not understood. This study was performed to test the role of NMDA-type glutamate receptors in spontaneous interbout arousal from hibernation. The most relevant and novel finding of this article is that signaling through an NMDA-type glutamate receptor plays a role in interbout arousal. This finding is important because glutamate, an excitatory neurotransmitter and derivative of α-ketoglutarate is poised to mediate crosstalk between metabolism and neural system processing and in this way translate metabolic needs into a neural response that signals interbout arousal.

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      Alterations in bioenergetic function induced by Parkinson’s disease mimetic compounds: lack of correlation with superoxide generation (pages 941–951)

      Brian P. Dranka, Jacek Zielonka, Anumantha G. Kanthasamy and Balaraman Kalyanaraman

      Article first published online: 11 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07836.x

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      Both mitochondrial dysfunction and increased oxidant production are implicated in Parkinson’s disease pathogenesis, though the causal relationship between these events is still under debate. Here, we found no correlation between mitochondrial dysfunction and superoxide levels in N27 cells treated with four toxicants known to cause PD-like symptoms in rodents. Instead, our data support a mechanism where mitochondrial dysfunction and superoxide production merely co-occur.

    6. Neuroinflammation & Neuroimmunology

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      Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE2 production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis (pages 952–961)

      Jin Hee Shin, Young Ae Lee, Jae Keun Lee, Yong Beom Lee, Woong Cho, Doo Soon Im, Jin Hwan Lee, Bok Sun Yun, Joe E. Springer and Byoung Joo Gwag

      Article first published online: 23 MAY 2012 | DOI: 10.1111/j.1471-4159.2012.07771.x

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      Targeting both free radicals and mPGES-1 in ALS This study was carried out to examine the pathologic roles of both free radicals and mPGES-1-mediated inflammation in a murine model of ALS. AAD-2004 prevents free radical production and mPGES-1-mediated PGE2 formation at nanomolar concentrations and shows better efficacy than ibuprofen and riluzole without causing gastric damage. Targeting both free radicals and mPGES-1-mediated inflammation sheds light on novel medications for ALS patients.

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      P-glycoprotein trafficking at the blood–brain barrier altered by peripheral inflammatory hyperalgesia (pages 962–975)

      Gwen McCaffrey, William D. Staatz, Lucy Sanchez-Covarrubias, Jessica D. Finch, Kristen DeMarco, Mei-Li Laracuente, Patrick T. Ronaldson and Thomas P. Davis

      Article first published online: 10 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07831.x

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      This study investigated the role of protein trafficking in the acute increase in P-glycoprotein efflux function at the blood–brain barrier (BBB) following the onset of peripheral inflammatory pain. P-glycoprotein constitutively incorporates within high molecular weight complexes, and peripheral inflammatory pain promotes structural changes in P-glycoprotein, such that it is released from storage and trafficked to the microvascular endothelial luminal plasma membrane where it is able to inhibit brain entry of drugs, such as morphine, that are clinically relevant to the treatment of pain states. The existence within cerebral microvascular endothelial cells of subcellular stores of P-glycoprotein, and the ability of a specific physiological condition, i.e., peripheral inflammatory pain, to promote release of “stored” P-glycoprotein, identifies novel targets for pharmacological modulation of the amount of P-glycoprotein present at the luminal plasma membrane to negatively impact drug delivery to the brain and central nervous system.

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      Harnessing pain heterogeneity and RNA transcriptome to identify blood-based pain biomarkers: a novel correlational study design and bioinformatics approach in a graded chronic constriction injury model (pages 976–994)

      Peter M. Grace, Daniel Hurley, Daniel T. Barratt, Anna Tsykin, Linda R. Watkins, Paul E. Rolan and Mark R. Hutchinson

      Article first published online: 9 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07833.x

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      Graded chronic constriction injury was performed in order to generate graded pain behavior. The transcriptomes were then collected from the whole blood and lumbar spinal dorsal quadrant, ipsilateral to the site of injury. Correlational analyses were designed to identify whole blood genes that were correlated with pain behavior and formed signaling pathways with lumbar spinal genes. Of the whole blood genes that fulfilled these criteria, a selection was confirmed in a subsequent validation study.

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      Chronic exposure to corticosterone enhances the neuroinflammatory and neurotoxic responses to methamphetamine (pages 995–1009)

      Kimberly A. Kelly, Diane B. Miller, John F. Bowyer and James P. O’Callaghan

      Article first published online: 3 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07864.x

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      Amphetamines, brain inflammation and neurotoxicity … stress may make a bad situation worseSystemic methamphetamine (METH) exposure causes large increases in striatal proinflammatory cytokines/chemokines and subsequent astrocytic hypertrophy, microglial activation, and dopaminergic nerve terminal damage. In an effort to evaluate the potential role of neuroinflammation in this neurotoxicity, we attempted to suppress the inflammation with the classic anti-inflammatory glucocorticoid, corticosterone (CORT).  Surprisingly, when pre-treated with chronic CORT, an enhanced striatal neuroinflammatory response to METH was observed, an effect that was accompanied by enhanced METH-induced gliosis and dopaminergic neurotoxicity. Chronic CORT pre-treatment also sensitized the frontal cortex and hippocampus to mount a neuroinflammatory response to METH.  These findings imply that chronic stress may make the CNS more susceptible to amphetamine and other neurotoxic exposures.

    10. Molecular Basis of Disease

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      Huntingtin associated protein 1 regulates trafficking of the amyloid precursor protein and modulates amyloid beta levels in neurons (pages 1010–1022)

      Gui-Zhi Yang, Miao Yang, Yoon Lim, Jian-Jun Lu, Ting-Hua Wang, Jian-Guo Qi, Jin-Hua Zhong and Xin-Fu Zhou

      Article first published online: 20 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07845.x

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      Trafficking and processing of APP is closely related to production of amyloid beta and Alzheimer’s disease but how APP is trafficked is not clear. HAP1 is physically associated with APP, regulates APP trafficking to non-amyloidogenic pathway and reduces A-beta production. HAP1 may be involved in the pathogenesis of Alzheimer’s disease.

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      β-Amyloid 1-42 induces physiological transcriptional regulation of BACE1 (pages 1023–1031)

      Alessandra Piccini, Roberta Borghi, Michela Guglielmotto, Elena Tamagno, Gabriella Cirmena, Anna Garuti, Valeria Pollero, Sergio Cammarata, Michele Fornaro, Massimo Messa, Laura Colombo, Mario Salmona, George Perry and Massimo Tabaton

      Article first published online: 11 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07834.x

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      Monomeric β-Amyloid 1-42 promotes gene transcriptionThe study was carried out to explain the mechanism of the over-expression of BACE1 induced by Aβ 1-42, previously shown by our research group. We describe that the monomeric peptide activates the expression of BACE1 without producing toxicity. Thus, Aβ 1-42 (but not Aβ 1-40) has a physiological effect on gene transcription, possibly in response to cellular stress. The excess of this function may be a major cause of Alzheimer’s disease.

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      Aging of the dopaminergic system and motor behavior in mice intoxicated with the parkinsonian toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pages 1032–1046)

      Sophie Schumm, Claude Sebban, Charles Cohen-Salmon, Jacques Callebert, Jean-Marie Launay, Jean-Louis Golmard, Lydie Boussicault, Isabelle Petropoulos, Audrey Hild, Estelle Rousselet, Annick Prigent, Bertrand Friguet, Jean Mariani and Etienne C. Hirsch

      Article first published online: 11 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07837.x

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      Aging is does not exacerbate Parkinson’s disease in miceBackground: The most important risk factor for Parkinson’s disease is aging but so far the effect of age on degeneration has not been studied in animal models. Findings: The study shows that aging does not exacerbate degeneration or symptoms in mice intoxicated by the parkinsonian toxin MPTP. Conclusions: These findings do not support the notion that PD develops with age after MPTP intoxication. Photographs of sections of the mesencephalon at 3 months in control mice and MPTP-intoxicated mice, respectively, (a–b) and 21 months (c–d). Evolution with age of dopaminergic and cresyl violet cell count (e,f) Semi-circle delimits SNpc and arrow shows SNpr; scale bar = 240 μm (a–f). Data are presented as mean ± SEM; *p < 0.05.

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      Long-term expression of glial cell line-derived neurotrophic factor slows, but does not stop retinal degeneration in a model of retinitis pigmentosa (pages 1047–1053)

      Masayuki Ohnaka, Katsuaki Miki, Yuan-Yuan Gong, Rebecca Stevens, Takeshi Iwase, Sean F. Hackett and Peter A. Campochiaro

      Article first published online: 23 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07842.x

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      Over-expression of GDNF; a single, not home run, for retinitis pigmentosaThis study was performed to determine the long-term effects of over-expression of GDNF in photoreceptors or retinal pigmented epithelium (RPE) in a model of retinitis pigmentosa (RP). Expression of GDNF in either cell type resulted in significant slowing of loss of function and death of both rods and cones, but did not prevent it. These data suggest that gene transfer of GDNF could be a useful adjunctive therapy, but by itself will only delay ultimate loss of vision.

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      Fluoxetine potentiation of methylphenidate-induced neuropeptide expression in the striatum occurs selectively in direct pathway (striatonigral) neurons (pages 1054–1064)

      Vincent Van Waes, Betsy Carr, Joel A. Beverley and Heinz Steiner

      Article first published online: 23 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07852.x

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      Potentiation of psychostimulant-induced gene regulation by SSRI antidepressants Pharmacotherapies combining SSRI antidepressants with the psychostimulant methylphenidate (Ritalin) are increasingly used to treat several mental disorders, but the molecular consequences of these combination treatments are poorly understood. This study demonstrates that the SSRI fluoxetine potentiates addiction-related gene regulation by methylphenidate in the basal ganglia. This finding suggests that SSRIs may enhance the addiction liability of methylphenidate.

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      Near-complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase (pages 1065–1080)

      Vladimir Farar, Franziska Mohr, Marie Legrand, Boris Lamotte d’Incamps, Jan Cendelin, Jacqueline Leroy, Marc Abitbol, Veronique Bernard, Frédéric Baud, Vincent Fournet, Pascal Houze, Jochen Klein, Benoit Plaud, Jan Tuma, Martina Zimmermann, Philippe Ascher, Anna Hrabovska, Jaromir Myslivecek and Eric Krejci

      Article first published online: 3 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07856.x

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      Mice lacking central acetylcholinesterase (AChE) adapt to this deficit and show very few physiological defects. Surprisingly, however, they are strongly affected by donepezil, a clinically used AChE inhibitor often assumed to act selectively on central AChE. The effect of donepezil in the knockout mice involves the AChE of the autonomic nervous system, which thus appears as a major pharmacological target.

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      Phosphorylation of Munc18-1 by Dyrk1A regulates its interaction with Syntaxin 1 and X11α (pages 1081–1091)

      Jung-Hwa Park, Min-Su Jung, Yeun-Soo Kim, Woo-Joo Song and Sul-Hee Chung

      Article first published online: 3 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07861.x

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      Phosphorylation of Munc18-1 by Dyrk1AMunc18-1, a central regulator of neurotransmitter release, interacts with Syntaxin and X11α. In this study, we showed that Dyrk1A phosphorylates Munc18-1 at the Thr479 residue in vitro and in vivo. This phosphorylation stimulates the binding of Munc18-1 to Syntaxin 1 and X11α, supporting the potential role of Dyrk1A-mediated phosphorylation in vesicle trafficking.

  5. CORRIGENDUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATIONS
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. ERRATUM
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      Corrigendum (page 1092)

      Article first published online: 9 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07851.x

      This article corrects:

      Differences in activation of ERK1/2 and p38 kinase in Jnk3 null mice following KA treatment

      Vol. 114, Issue 5, 1315–1322, Article first published online: 8 JUN 2010

  6. ERRATUM

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW
    4. SHORT COMMUNICATIONS
    5. ORIGINAL ARTICLES
    6. CORRIGENDUM
    7. ERRATUM
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      Erratum (page 1093)

      Article first published online: 3 JUL 2012 | DOI: 10.1111/j.1471-4159.2012.07854.x

      This article corrects:

      Sex differences in brain proteomes of neuron-specific STAT3-null mice after cerebral ischemia/reperfusion

      Vol. 121, Issue 4, 680–692, Article first published online: 28 MAR 2012

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