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Journal of Neurochemistry

Cover image for Journal of Neurochemistry

December 2011

Volume 119, Issue 6

Pages 1155–1343

  1. SHORT COMMUNICATION

    1. Top of page
    2. SHORT COMMUNICATION
    3. ORIGINAL ARTICLES
    4. ACKNOWLEDGEMENT OF REVIEWERS
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      HspB8 mutation causing hereditary distal motor neuropathy impairs lysosomal delivery of autophagosomes (pages 1155–1161)

      Alice S. Kwok, Kanchan Phadwal, Bradley J. Turner, Peter L. Oliver, Annie Raw, Anna Katharina Simon, Kevin Talbot and Vishwas R. Agashe

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07521.x

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      HspB8 Mutation Causing Hereditary Distal Motor Neuropathy Impairs Lysosomal Delivery of Autophagosomes Mutations in HspB8, a protein implicated in macroautophagy, cause distal hereditary motor neuropathy type II (dHMNII). In motor neuron-like cells mutant HspB8 was found to initiate autophagy but not bring it to completion. We found a similar autophagy impairment in isolated peripheral blood mononuclear cells of dHMNII patients that could act as a biomarker and indicates that an autophagy defect may contribute to pathogenesis.

  2. ORIGINAL ARTICLES

    1. Top of page
    2. SHORT COMMUNICATION
    3. ORIGINAL ARTICLES
    4. ACKNOWLEDGEMENT OF REVIEWERS
    1. Signal Transduction & Synaptic Transmission

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      High doses of amphetamine augment, rather than disrupt, exocytotic dopamine release in the dorsal and ventral striatum of the anesthetized rat (pages 1162–1172)

      Eric S. Ramsson, Christopher D. Howard, Dan P. Covey and Paul A. Garris

      Version of Record online: 25 AUG 2011 | DOI: 10.1111/j.1471-4159.2011.07407.x

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      Amphetamine: old drug…new mechanism This study investigated the mechanism of amphetamine, an addictive drug with a clinical relevance for treating attention-deficit hyperactivity disorder. The major result was that amphetamine augmented exocytotic dopamine release, challenging the current dogma that the primary actions of amphetamine are depletion of vesicular dopamine stores and non-exocytotic dopamine efflux.

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      The chemokine BRAK/CXCL14 regulates synaptic transmission in the adult mouse dentate gyrus stem cell niche (pages 1173–1182)

      Ghazal Banisadr, Bula J. Bhattacharyya, Abdelhak Belmadani, Sarah C. Izen, Dongjun Ren, Phuong B. Tran and Richard J. Miller

      Version of Record online: 2 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07509.x

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      How do cytokines regulate neurogenesis? The chemokine CXCL14 is highly expressed in the nervous system but what does it do? We found that CXCL14 was expressed by GABAergic interneurons in the dentate gyrus. CXCL14 inhibited and CXCL12 enhanced GABAergic transmission to neural progenitor cells in the dentate gyrus. Hence, CXCL14 and CXCL12 may act as up and down regulators of neurogenesis in the dentate gyrus.

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      Neuronal Nogo-A regulates glutamate receptor subunit expression in hippocampal neurons (pages 1183–1193)

      Xiangmin Peng, Jeeyong Kim, Zhigang Zhou, David J. Fink and Marina Mata

      Version of Record online: 2 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07520.x

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      NogoA expressed in oligodendrocytes inhibits axonal extension (hence ‘Nogo’). We show that NogoA expressed in mature neurons, acting through the NogoR1 receptor regulates NMDA and AMPA receptor subunit expression by a rapamycin-sensitive mTOR pathway. Thus, NogoA/NogoR1 has two functions: one in regulating axon elongation and the other in regulating synaptic function.

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      The phosphorylation status of extracellular-regulated kinase 1/2 in astrocytes and neurons from rat hippocampus determines the thrombin-induced calcium release and ROS generation (pages 1194–1204)

      Gregor Zündorf and Georg Reiser

      Version of Record online: 10 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07527.x

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      Protease-activated receptors (PAR) induce cytosolic Ca2+ concentration ([Ca2+]c) increase, mitogen-activated protein kinase activation and reactive oxygen species (ROS) formation with a bandwidth of responses in individual hippocampal cells. In this in situ study, we show that the phosphorylation status of ERK1/2 in dissociated hippocampal astrocytes and neurons in a mixed culture determines the magnitude and time course of thrombin-dependent [Ca2+]c increase and ROS formation and, thus, influences the capacity of thrombin to regulate neuroprotection or neurodegeneration.

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      Developmental changes of TrkB signaling in response to exogenous brain-derived neurotrophic factor in primary cortical neurons (pages 1205–1216)

      Xianju Zhou, Hua Xiao and Hongbing Wang

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07528.x

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      Declines of BDNF-TrkB signaling during in vitro maturation Previous studies implicate that BDNF signaling and GABAergic inhibition may control the timing of the critical period, after which neurons become less sensitive to external stimuli. We found that the increased GABAergic inhibition correlated with the decline of BDNF-mediated activation of ERK1/2-CREB cascade in older neurons. The less dynamic molecular responses may be relevant to the loss of plasticity during maturation.

    6. Brain Development & Cell Differentiation

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      Regeneration of dopaminergic neurons after 6-hydroxydopamine-induced lesion in planarian brain (pages 1217–1231)

      Kaneyasu Nishimura, Takeshi Inoue, Kanji Yoshimoto, Takashi Taniguchi, Yoshihisa Kitamura and Kiyokazu Agata

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07518.x

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      Planarians regenerate dopaminergic neurons after selective degeneration of these neurons by treatment with 6-hydroxydopamine. This suggests that planarians have a system to sense the degeneration of dopaminergic neurons and to recruit stem cells to produce dopaminergic neurons to recover their function. New findings obtained from planarian regeneration provide hints about how to conduct cell-transplantation therapy for future regenerative medicine.

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      Neuritogenic activity of a genipin derivative in retinal ganglion cells is mediated by retinoic acid receptor β expression through nitric oxide/S-nitrosylation signaling (pages 1232–1242)

      Yoshiki Koriyama, Yusuke Takagi, Kenzo Chiba, Matsumi Yamazaki, Kunizo Arai, Toru Matsukawa, Hirokazu Suzuki, Kayo Sugitani, Hiroyuki Kagechika and Satoru Kato

      Version of Record online: 9 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07533.x

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      A novel target for glaucomatous condition? Genipin, a herbal iridoid, has neuroprotective and neuritogenic activities. We previously proposed a novel neuroprotective activity of a genipin derivative, (1R)-isoPropyloxygenipin (IPRG001), whereby it reduces oxidative stress in RGC-5, a neuronal precursor cell line of retinal origin. IPRG001 stimulates neurite outgrowth in RGC-5 culture through nitric oxide-dependent signaling, requiring retinoic acid receptor β (RARβ) expression presumably mediated by protein S-nitrosylation. Genipin could be a new target for RGC regeneration after glaucomatous condition.

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      Excitotoxicity-induced endocytosis mediates neuroprotection by TAT-peptide-linked JNK inhibitor (pages 1243–1252)

      Anne Vaslin, Sonia Naegele-Tollardo, Julien Puyal and Peter G. H. Clarke

      Version of Record online: 9 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07535.x

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      Excitotoxicity-induced endocytosis provides specific drug-targeting for neuroprotection. There is currently no neuroprotective pharmacotherapy for stroke. This is partly because of drug side-effects, but these might be reduced if delivery specificity could be increased. We recently showed that TAT peptides can be targeted to the cells that need them by excitotoxicity-induced endocytosis, which is clathrin/dynamin-dependent. Our present study shows that excitotoxicity-induced endocytosis of a TAT-linked JNK-inhibitory peptide gives neuroprotection, whereas constitutive endocytosis does not.

    9. Bioenergetics & Metabolism

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      Isolation of brain mitochondria from neonatal mice (pages 1253–1261)

      Xiaoyang Wang, Anna-Lena Leverin, Wei Han, Changlian Zhu, Bengt R. Johansson, Etienne Jacotot, Vadim S. Ten, Neil R. Sims and Henrik Hagberg

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07525.x

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      A comparison of methods to isolate brain mitochondria Mitochondria are key contributors to many forms of cell death including those resulting from neonatal hypoxic-ischemic brain injury. This study provides a comparison of a previously published procedure for isolating mitochondria from neonatal mouse brain (method A) with procedures adapted from those for adult rats (method B) and neonatal rats (method C) and discusses advantages and disadvantages of the three methods.

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      Amlodipine besylate and amlodipine camsylate prevent cortical neuronal cell death induced by oxidative stress (pages 1262–1270)

      Young Joo Lee, Hyun-Hee Park, Seong-Ho Koh, Na-Young Choi and Kyu-Yong Lee

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07529.x

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      A very brief graphical abstract for "Amlodipine Besylate and Amlodipine Camsylate Prevent Cortical Neuronal Cell Death Induced by Oxidative Stress" This study was performed to examine the neuroprotective effects of amlodipine besylate (AB) and amlodipine camsylate (AC). AB and AC exert neuroprotective effects by reducing oxidative stress, enhancing survival signals, and inhibiting death signals. AB and AC may have applications as neuroprotective agents in addition to their effects on blood pressure in hypertensive patients.

    11. Neuronal Plasticity & Behavior

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      A morphine/heroin vaccine with new hapten design attenuates behavioral effects in rats (pages 1271–1281)

      Qian-Qian Li, Yi-Xiao Luo, Cheng-Yu Sun, Yan-Xue Xue, Wei-Li Zhu, Hai-Shui Shi, Hai-Feng Zhai, Jie Shi and Lin Lu

      Version of Record online: 28 OCT 2011 | DOI: 10.1111/j.1471-4159.2011.07502.x

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      Novel vaccine blocks morphine/heroin relapse Immunotherapy has shown efficacy in preventing nicotine and cocaine relapse in clinical trials. Here reported a novel morphine conjugate vaccine, including a novel hapten, 6-glutarylmorphin, with keyhole limpet hemocyanin (KLH), triggered a robust and specific antibody response sufficient to attenuate behavioral and psychoactive effects of morphine/heroin in rats. This vaccine might potentially be implicated in the clinical treatment of opiate abuse.

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      Environmental enrichment compensates for the effects of stress on disease progression in Tg2576 mice, an Alzheimer’s disease model (pages 1282–1293)

      Yun Ha Jeong, Joon Min Kim, Jongman Yoo, Sang Hyung Lee, Hye-Sun Kim and Yoo-Hun Suh

      Version of Record online: 9 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07514.x

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      This study, performed to determine whether environmental factors can modulate the progress of AD, shows that environmental enrichment counteracts the effect of stress on cognitive deficits and pathology in AD. Environmental factors are thus important as a major modulator for the disease progression of ADs measured by expression of tau protein, learning and memory deficits and neurogenesis.

    13. Molecular Basis of Disease

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      Catecholamines up integrates dopamine synthesis and synaptic trafficking (pages 1294–1305)

      Zhe Wang, Faiza Ferdousy, Hakeem Lawal, Zhinong Huang, J. Gavin Daigle, Iyare Izevbaye, Olugbenga Doherty, Jerrad Thomas, Dean G Stathakis and Janis M. O’Donnell

      Version of Record online: 3 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07517.x

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      Catecholamines up integrates dopamine synthesis and synaptic trafficking The highly reactive nature of dopamine heightens the oxidative risk of dopaminergic neurons. Mutations in the Drosophila gene Catecholamines up (Catsup), however, cause dominantly elevated dopamine pools, while increasing resistance to oxidative stress. This study demonstrates that Catsup regulates and coordinates dopamine synthesis and synaptic trafficking. This novel integration function has important implications for dopamine modulated behaviors and susceptibility to dopamine-linked disorders.

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      Ethanol increases p190RhoGAP activity, leading to actin cytoskeleton rearrangements (pages 1306–1316)

      Javier Selva and Gustavo Egea

      Version of Record online: 2 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07522.x

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      Ethanol induces severe rearrangements in the actin cytoskeleton in newborn rat astrocytes. Such rearrangements resulted from an increase in the total RhoGAP activity. Here, we show that ethanol stimulates the recruitment of p190RhoGAPs (p190A and p190B) to the plasma membrane, where they are activated either by phosphorylation, interaction with p120RasGAP or both. We reveal p190RhoGAPs as a potential therapeutical target against Foetal Alcohol Spectrum Disorders.

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      Antiangiogenic effects of β2-adrenergic receptor blockade in a mouse model of oxygen-induced retinopathy (pages 1317–1329)

      Davide Martini, Massimo Dal Monte, Chiara Ristori, Elena Cupisti, Sara Mei, Patrizio Fiorini, Luca Filippi and Paola Bagnoli

      Version of Record online: 2 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07530.x

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      β-adrenoreceptors play a major role in retinal angiogenesis.This study is the first attempt to investigate the role of β-adrenoreceptors in oxygen-induced retinopathy, a model of retinopathy of prematurity. β2-adrenoreceptor blockade ameliorates proangiogenic factors, retinal neovascularization and electroretinogram in response to hypoxia. These findings suggest that β2-adrenoreceptor activation constitutes an important part of retinal responses to hypoxia and indicate that β2-adrenoreceptor blockade is effective against retinal dysfunction.

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      A novel glycogen synthase kinase-3 inhibitor 2-methyl-5-(3-{4-[(S )-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole decreases tau phosphorylation and ameliorates cognitive deficits in a transgenic model of Alzheimer’s disease (pages 1330–1340)

      Tomohiro Onishi, Hiroki Iwashita, Yumiko Uno, Jun Kunitomo, Morihisa Saitoh, Eiji Kimura, Hisashi Fujita, Noriko Uchiyama, Masakuni Kori and Masayuki Takizawa

      Version of Record online: 2 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07532.x

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      A novel glycogen synthase kinase-3 inhibitor MMBO shows therapeutic effects in AD mouse model. Glycogen synthase kinase-3 (GSK-3) is involved in AD pathogenesis as one of tau kinases. We report that a novel selective GSK-3 inhibitor MMBO lowers tau phosphorylation in vitro and in vivo, and ameliorates AD-like symptoms in AD mouse model. These results indicate that MMBO and the resultant decrease in tau phosphorylation may represent a valid therapeutic strategy for AD.

  3. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. SHORT COMMUNICATION
    3. ORIGINAL ARTICLES
    4. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
      Acknowledgement of Reviewers (pages 1341–1343)

      Version of Record online: 9 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07568.x

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