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Journal of Neurochemistry

Cover image for Vol. 127 Issue 2

October 2013

Volume 127, Issue 2

Pages i–x, 149–298

  1. IN THIS ISSUE

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. ORIGINAL ARTICLES
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      In this Issue (pages i–x)

      Version of Record online: 4 OCT 2013 | DOI: 10.1111/jnc.12449

  2. EDITORIAL HIGHLIGHT

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. ORIGINAL ARTICLES
    1. You have free access to this content
      Up-regulation of sortilin mediated by amyloid-β and p75NTR: safety lies in the middle course (pages 149–151)

      Elizabeth J. Coulson and Anders Nykjaer

      Version of Record online: 28 AUG 2013 | DOI: 10.1111/jnc.12389

      Read the full articleAmyloid beta1–42 (Aβ42) up- regulates the expression of sortilin via the p75NTR/RhoA signaling pathway’ on doi: 10.1111/jnc.12383

  3. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. EDITORIAL HIGHLIGHT
    4. ORIGINAL ARTICLES
    1. Gene Regulation & Genetics

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      Amyloid beta1–42 (Aβ42) up-regulates the expression of sortilin via the p75NTR/RhoA signaling pathway (pages 152–162)

      Khalil Saadipour, Miao Yang, Yoon Lim, Kristen Georgiou, Ying Sun, Damien Keating, Jia Liu, Ye-Ran Wang, Wei-ping Gai, Jin-hua Zhong, Yan-Jiang Wang and Xin-Fu Zhou

      Version of Record online: 22 AUG 2013 | DOI: 10.1111/jnc.12383

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      Sortilin is the co-receptor of p75NTR which signals the cell death induced by Aβ and proneurotrophins. We found that sortilin is increased in the AD brain and up-regulated by Aβ and pro-brain-derived neurotrophic factor (proBDNF). Aβ-induced upregulation of sortilin is mediated by p75NTR and the down-streaming RhoA-ROCK signaling pathway. The Aβ/Sortilinp/75NTR signaling may play a role in the pathogenesis of AD.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.12389.

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      Crosstalk between Dopamine D2 receptors and cannabinoid CB1 receptors regulates CNR1 promoter activity via ERK1/2 signaling (pages 163–176)

      Yao-Chang Chiang, Yan-Ni Lo and Jin-Chung Chen

      Version of Record online: 28 AUG 2013 | DOI: 10.1111/jnc.12399

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      Cannabinoid CB1R and dopamine D2R cross-talk at ERK1/2 signal. Activation of D2SR increases the CB1R transcription, which is ERK1/2 dependent and enhances CB1R promoter activity that requires up-stream −1 to −222 region. The results implicate pre-synaptic D2SR could functionally regulate the retrograde cannabinoid signal in the striatum.

    3. Signal Transduction & Synaptic Transmission

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      GZ-793A, a lobelane analog, interacts with the vesicular monoamine transporter-2 to inhibit the effect of methamphetamine (pages 177–186)

      David B. Horton, Justin R. Nickell, Guangrong Zheng, Peter A. Crooks and Linda P. Dwoskin

      Version of Record online: 19 AUG 2013 | DOI: 10.1111/jnc.12371

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      GZ-793A inhibits methamphetamine-evoked dopamine release from synaptic vesicles through a surmountable allosteric mechanism and interacts with several sites on the vesicular monoamine transporter-2 (VMAT2), including high- and-low affinity intravesicular dopamine release sites, high-affinity extravesicular dopamine uptake sites and low-affinity extravesicular dihydrotetrabenazine binding sites. VMAT2 interactions likely underlie the ability of GZ-793A to attenuate the neurochemical and behavioral effects of methamphetamine.

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      Effects of VMAT2 inhibitors lobeline and GZ-793A on methamphetamine-induced changes in dopamine release, metabolism and synthesis in vivo (pages 187–198)

      Andrew C. Meyer, Nichole M. Neugebauer, Guangrong Zheng, Peter A. Crooks, Linda P. Dwoskin and Michael T. Bardo

      Version of Record online: 20 AUG 2013 | DOI: 10.1111/jnc.12373

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      We determined if inhibition of the vesicular monoamine transporter (VMAT2) alters METH-induced changes in dopamine (DA) release, metabolism, and synthesis in vivo. Our results suggest that selective inhibition of VMAT2 produces a time-dependent decrease in DA release as a result of alterations in tyrosine hydroxylase (TH) activity, which may play a role in the ability of the VMAT2 inhibitor GZ-793A to decrease METH reward.

    5. Brain Development & Cell Differentiation

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      Galanin stimulates neurite outgrowth from sensory neurons by inhibition of Cdc42 and Rho GTPases and activation of cofilin (pages 199–208)

      Sally-Ann Hobson, Penny A. Vanderplank, Robert J. P. Pope, Niall C. H. Kerr and David Wynick

      Version of Record online: 22 AUG 2013 | DOI: 10.1111/jnc.12379

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      Galanin plays a key role in neurite outgrowth from adult sensory neurons via activation of the second galanin receptor (GalR2). Our results demonstrate the galanin decreases the activation state of Rho and Cdc42 and markedly increases the activation of cofilin. These changes lead to alterations in growth cone motility. These findings have important implications for the treatment of peripheral sensory neuropathies.

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      GalR3 activation promotes adult neural stem cell survival in response to a diabetic milieu (pages 209–220)

      Shiva Mansouri, Swapnali Barde, Henrik Ortsäter, Mohamed Eweida, Vladimer Darsalia, Ülo Langel, Åke Sjöholm, Tomas Hökfelt and Cesare Patrone

      Version of Record online: 3 SEP 2013 | DOI: 10.1111/jnc.12396

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      Adult neurogenesis impairment in diabetes could play a role in the development of neurological complications. GalR3 activation counteracts glucolipotoxicity in adult neural stem cells (NSCs) in the subventricular zone (SVZ) by decreasing apoptosis. At least part of the protective effect mediated by GalR3 activation occurs through modulation of the unfolded protein response (UPR) signaling in the endoplasmic reticulum. The data support a potential therapeutic development for treatment of diabetic brain disorders, based on increased neurogenesis by GalR3 activation. CB, cerebellum; LV, lateral ventricle; OB, olfactory bulb.

    7. Neuroinflammation & Neuroimmunology

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      Mitochondrial dynamics modulate the expression of pro-inflammatory mediators in microglial cells (pages 221–232)

      Junghyung Park, Hoonsung Choi, Ju-Sik Min, Sun-Ji Park, Jung-Hak Kim, Hyo-Jin Park, Bokyung Kim, Jung-Il Chae, Mijung Yim and Dong-Seok Lee

      Version of Record online: 29 JUL 2013 | DOI: 10.1111/jnc.12361

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      LPS induced excessive mitochondrial fission through mitochondrial localization of de-phosphorylation of Ser637 Drp1. Interestingly, inhibition of LPS-induced mitochondrial fission and mitochondrial ROS generation by Mdivi-1 and Drp1 shRNA attenuate the production of pro-inflammatory mediators via reduced NF-κB and MAPK signaling. Our results suggest that mitochondrial dynamics may be essential for understanding pro-inflammatory mediator expression in activated microglial cells.

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      Interleukin-1β orchestrates underlying inflammatory responses in microglia via Krüppel-like factor 4 (pages 233–244)

      Deepak K. Kaushik, Menaka C. Thounaojam, Kanhaiya L. Kumawat, Malvika Gupta and Anirban Basu

      Version of Record online: 19 AUG 2013 | DOI: 10.1111/jnc.12382

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      IL-1β is a potent pro-inflammatory cytokine which regulates inflammation in brain via activation of microglia. In this regard, we unravelled mechanisms for IL-1β mediated regulation of downstream Cox-2, iNOS (inducible nitric oxide synthase) as well as other cyto-chemokines in microglia and have established a role for Klf4 in mediating microglial activation. We further report that Klf4 mediates the production of endogenous IL-1β in response to exogenous IL-1β stimulation. We hereby propose a novel transcription factor underlying IL-1β mediated modulation of inflammation in the CNS.

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      Microglia in juvenile neuronal ceroid lipofuscinosis are primed toward a pro-inflammatory phenotype (pages 245–258)

      Juan Xiong and Tammy Kielian

      Version of Record online: 22 AUG 2013 | DOI: 10.1111/jnc.12385

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      Juvenile neuronal ceroid lipofuscinosis (JNCL) is a lysosomal storage disease caused by an autosomal recessive mutation in CLN3. Regions of microglial activation precede and predict areas of neuronal loss in JNCL; however, the functional role of activated microglia remains to be defined. In this report, primary microglia from CLN3Δex7/8 mutant mice over-produced numerous inflammatory cytokines in response to stimuli that are present in the JNCL brain, whereas wild-type microglia were relatively non-responsive. In addition, activated microglia induced significant cell death in CLN3Δex7/8 but not wild-type neurons, demonstrating that intrinsically diseased CLN3Δex7/8 neurons are less equipped to withstand cytotoxic insults. Collectively, aberrant microglial activation may contribute to the pathological chain of events leading to neurodegeneration during later stages of JNCL.

    10. Molecular Basis of Disease

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      Minocycline reduces remyelination by suppressing ciliary neurotrophic factor expression after cuprizone-induced demyelination (pages 259–270)

      Tatsuhide Tanaka, Koichi Murakami, Yoshio Bando and Shigetaka Yoshida

      Version of Record online: 20 MAY 2013 | DOI: 10.1111/jnc.12289

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      To examine the role of microglia in remyelination, mice were treated with minocycline after cuprizone-induced demyelination. Minocycline treatment reduced the number of oligodendrocytes and CNTF expression in the remyelination phase. In vitro, CNTF directly affected the differentiation of oligodendrocytic cells. These findings suggest that minocycline reduces remyelination by suppressing CNTF expression by microglia after cuprizone-induced demyelination.

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      Diethylmaleate and iodoacetate in combination caused profound cell death in astrocytes (pages 271–282)

      Su-Lan Liao, Yen-Chuan Ou, Cheng-Yi Chang, Wen-Ying Chen, Yu-Hsiang Kuan, Wen-Yi Wang, Hung-Chuan Pan and Chun-Jung Chen

      Version of Record online: 20 MAY 2013 | DOI: 10.1111/jnc.12291

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      Energy failure and oxidative stress have been implicated in the pathogenesis of ischemia and cell death. Through the application of the glycolytic inhibitor iodoacetate and the glutathione chelator diethylmaleate, we report a potential link between cytosolic phospholipase A2 (cPLA2) activation and energy failure/oxidative stress-induced astrocyte damage involving reactive oxygen species (ROS), signaling through the kinases PKC-α, Src, Raf, and ERK and concurrent elevation of endogenous chelatable zinc.

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      Kallikrein 6 signals through PAR1 and PAR2 to promote neuron injury and exacerbate glutamate neurotoxicity (pages 283–298)

      Hyesook Yoon, Maja Radulovic, Jianmin Wu, Sachiko I. Blaber, Michael Blaber, Michael G. Fehlings and Isobel A. Scarisbrick

      Version of Record online: 27 MAY 2013 | DOI: 10.1111/jnc.12293

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      Here, we show kallikrein 6 (Klk6) and thrombin contribute to the proteolytic imbalance that occurs in CNS injury. Activation of the G-protein coupled receptor PAR1 was sufficient to mediate the neurotoxic effects of thrombin while KLK6 neurotoxicity involved activation of PAR1 and PAR2. In addition, both proteases exacerbated glutamate neurotoxicity. These data suggest Klk6, thrombin and PARs each represent new targets for the development of neuroprotective therapies.

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