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Journal of Neurochemistry

Cover image for Vol. 120 Issue 4

February 2012

Volume 120, Issue 4

Pages 475–640

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
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  2. REVIEW ARTICLE

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. You have free access to this content
  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLE
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. You have free access to this content
      Activity-dependent survival of developing neocortical neurons depends on PI3K signalling (pages 495–501)

      Antje Wagner-Golbs and Heiko J. Luhmann

      Article first published online: 15 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07591.x

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      This study addressed the question how physiologically relevant spontaneous electrical activity patterns control the process of programmed cell death in the developing cerebral cortex. Using organotypic slice cultures showing different activity patterns, we demonstrate that the PI3K/Akt, but not the Ras/MEK/ERK or CaM/CaMK, pathway control the caspase 3 dependent apoptotic cell death. These data indicate that any perturbation in early electrical activity patterns may have an impact on the regulation of programmed cell death in the developing brain.

  4. ORIGINAL ARTICLES

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

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      Cholesterol enhances neuron susceptibility to apoptotic stimuli via cAMP/PKA/CREB-dependent up-regulation of Kv2.1 (pages 502–514)

      Meng-Hua Zhou, Guang Yang, Song Jiao, Chang-Long Hu and Yan-Ai Mei

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07593.x

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      Cholesterol enhances neuron apoptosis and Kv2.1 expression Cholesterol enrichment potentiated rat cerebellar granule neurons (CGNs) apoptosis in 5 mM K+/serum free (LK-S) medium. Cholesterol depletion using MβCD protected CGNs from apoptosis. Cholesterol-treated CGNs also exhibited increased cAMP levels and up-regulation of Kv2.1 expression. Our results demonstrate that the elevation of membrane cholesterol enhances CGN susceptibility to apoptotic stimuli via cAMP/PKA/CREB-dependent up-regulation of Kv2.1. and provide new evidence for the role of cholesterol in neuronal apoptosis.

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      Cofilin activation mediates Bax translocation to mitochondria during excitotoxic neuronal death (pages 515–527)

      Inmaculada Posadas, Francisco C. Pérez-Martínez, Javier Guerra, Prado Sánchez-Verdú and Valentín Ceña

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07599.x

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      Cofilin plays a key role in excitotoxic death This study was performed to identify the role of cofilin in excitotoxic death by knocking down cofilin and the phosphatases that activate it using dendrimer-delivered siRNA. The most relevant finding is that cofilin knock down using a dendrimer-delivered siRNA almost completely blocked excitotoxic neuronal death in rat cortical neurons, likely by inhibiting Bax translocation to the mitochondria. The conclusion is relevant because it unveils a new key signaling pathway in excitotoxic neuronal death that might be a therapeutic target in neurodegenerative diseases. In addition, the paper indicates that it is possible to dissect neuronal signaling pathways using dendrimer-delivered specific siRNA.

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      Comparison of Cbln1 and Cbln2 functions using transgenic and knockout mice (pages 528–540)

      Yongqi Rong, Peng Wei, Jennifer Parris, Hong Guo, Roberto Pattarini, Kristen Correia, Leyi Li, Sheila V. Kusnoor, Ariel Y. Deutch and James I. Morgan

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07604.x

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      Do Cbln1 and Cbln2 have redundant functions in vivo? Cbln1 is a bi-functional ligand that bridges neurexins on pre-synaptic membranes to Grid2 on post-synaptic membranes in cerebellum, thereby stabilizing granule cell-Purkinje cell synaptic interactions. By using transgenic and knockout mice, we show that Cbln2 can exhibit functional redundancy with Cbln1 in cerebellum but it does not have the same properties as Cbln1 in thalamic neurons, implying one or both ligands utilize different receptors/mechanisms in these two brain region.

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      Reduced calcium/calmodulin-dependent protein kinase II activity in the hippocampus is associated with impaired cognitive function in MPTP-treated mice (pages 541–551)

      Shigeki Moriguchi, Yasushi Yabuki and Kohji Fukunaga

      Article first published online: 6 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07608.x

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      Parkinson’s disease (PD) patients frequently reveal deficit in cognitive functions. Here, we demonstrated that deficits in cognitive functions in MPTP-treated mice were associated with reduced calcium/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and impaired LTP induction in the hippocampus. Concomitant with impaired LTP induction, CaMKII autophosphorylation was significantly decreased 1 week after MPTP treatment in DG and 3 to 4 weeks after MPTP treatment in CA1 and CA3 region. Thus, DA depletion induced by MPTP causes impairment of hippocampal DG region in early stage and CA1 or CA3 region was observed in the late stage.

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      Modulation of glutamate release from parallel fibers by mGlu4 and pre-synaptic GABAA receptors (pages 552–563)

      Jordan E. Antflick and David R. Hampson

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07611.x

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      Presynaptic GABA and Glutamate Receptors The purpose of this study was to determine if pre-synaptic mGlu4 and GABAA receptors in the cerebellum are associated and interact with each other. We found that these two receptors are co-localized in parallel fiber terminals and co-immunoprecipitate from cerebellar tissue. Based on functional analysis, we conclude that simultaneous co-activation of mGlu4 and GABAA receptors enhances glutamate release.

    6. Molecular Basis of Disease

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      Autophagosomes accumulation is associated with β-amyloid deposits and secondary damage in the thalamus after focal cortical infarction in hypertensive rats (pages 564–573)

      Jian Zhang, Yusheng Zhang, Jingjing Li, Shihui Xing, Chuo Li, Yiliang Li, Chao Dang, Yuhua Fan, Jian Yu, Zhong Pei and Jinsheng Zeng

      Article first published online: 20 OCT 2011 | DOI: 10.1111/j.1471-4159.2011.07496.x

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      Autophagy is an active pathway for β-amyloid peptide generation. Here, we investigated the role of autophagy in thalamic β-amyloid deposition and neuronal degeneration after cerebral cortical infarction. Our results indicated that autophagosomes accumulate within thalamic cells after cerebral cortical infarction, and the inhibition of autophagy with 3-methyladenine significantly reduced the thalamic β-amyloid deposits and neuronal damage. These findings suggest that autophagy may represent a novel target for the treatment of secondary thalamic damage after focal cortical infarction.

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      Why are hippocampal CA1 neurons vulnerable but motor cortex neurons resistant to transient ischemia? (pages 574–585)

      Hong Zhu, Tanihiro Yoshimoto, Shinobu Imajo-Ohmi, Maryia Dazortsava, Arumugam Mathivanan and Tetsumori Yamashima

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07550.x

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      A differential role of Hsp70.1 between motor cortex and CA1 neurons after ischemia/reperfusion Recently, we found that calpain-mediated cleavage of the carbonylated Hsp70.1 is crucial for the CA1 neuronal death after ischemia/reperfusion. We demonstrated here that Hsp70.1in motor cortex neurons lacking calpain activation can play a neuroprotection when compared with that in CA1, thus revealing a new mechanism underlying lysosomal stabilization and inhibiting NF-κB p65 activation by Hsp70.1 may influence neuronal survival /death.

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      Astroglial NF-κB mediates oxidative stress by regulation of NADPH oxidase in a model of retinal ischemia reperfusion injury (pages 586–597)

      David J. Barakat, Galina Dvoriantchikova, Dmitry Ivanov and Valery I. Shestopalov

      Article first published online: 4 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07595.x

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      A key role for astrocytes in regulating oxidative stress The role of NF-κB in ischemic retinal injury remains controversial because this transcription factor is known to contribute to both cell survival and neurotoxicity. Our results indicate that the outcome is cell type dependent, where astrocyte-specific activation of NF-κB triggers pro-apoptotic signaling in retinal ganglion cells through activation of NADPH oxidase. These data suggest a new mechanism for astroglial toxicity via NF-κB-mediated regulation of oxidative stress.

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      Paradoxical roles of serine racemase and d-serine in the G93A mSOD1 mouse model of amyotrophic lateral sclerosis (pages 598–610)

      Misty Thompson, John C. Marecki, Stephane Marinesco, Viviane Labrie, John C. Roder, Steven W. Barger and John P. Crow

      Article first published online: 4 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07601.x

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      Do glial cells use d-serine to kill motor neurons? d-Serine is produced by glia, and is excitotoxic by virtue of its ability to increase glutamate binding affinity at the NMDA-R. It is elevated in spinal cords of mhSOD1 ALS mice, and treatments which normalize it alter symptom onset and slow disease progression. These results suggest a fundamental connection between d-serine, hSOD1 mutants, and glial-mediated motor neuron death in ALS.

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      Mutant LGI1 inhibits seizure-induced trafficking of Kv4.2 potassium channels (pages 611–621)

      Stephen E. P. Smith, Lin Xu, Michael R. Kasten and Matthew P. Anderson

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07605.x

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      Anti-Seizure Channel Trafficking in Thalamus and Human Epilepsy Gene LGI1 Seizures traffic Kv4.2 potassium channel to the surface of thalamic relay neurons to inhibits excitatory synaptic transmission. In transgenic mice carrying a human epilepsy-associated dominant-negative mutant of LGI1 this response is blocked. The result uncovers a new anti-seizure mechanism in human LGI1 partial epilepsy.

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      DHA inhibits ER Ca2+ release and ER stress in astrocytes following in vitro ischemia (pages 622–630)

      Gulnaz Begum, Douglas Kintner, Yan Liu, Samuel W. Cramer and Dandan Sun

      Article first published online: 13 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07606.x

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      DHA attenuates ER stress in astrocytes. Astrocytes are the only brain cell type to synthesize docosahexaenoic acid (DHA). Its role in astrocyte function is not clear. DHA and its oxidized product NPD1 blocked IP3 receptor-mediated Ca2+ release from ER Ca2+ stores, ER stress, and astrocyte death following in vitro ischemia. This suggests that DHA enhances astrocyte tolerance against ischemic insult by preventing Ca2+ dysregulation and ER stress.

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      A specific multi-nutrient formulation enhances M1 muscarinic acetylcholine receptor responses in vitro (pages 631–640)

      Paul J. M. Savelkoul, Helena Janickova, Almar A. M. Kuipers, Robert J. J. Hageman, Patrick J. Kamphuis, Vladimir Dolezal and Laus M. Broersen

      Article first published online: 6 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07616.x

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      Nutrient formulation enhances M1 muscarinic acetylcholine receptor responses.As recent evidence indicates that supplementation with specific nutrients may affect cell membrane synthesis and composition, we investigated whether such nutrients may affect membrane-bound processes involved in signal transduction pathways. Our results indicate that a specific combination of nutrients acts synergistically in enhancing muscarinic M1 receptor responses in vitro. The data support the use of a membrane-targeting dietary intervention to influence M1 receptor functioning, relevant for Alzheimer’s pathology and memory performance.

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