European Journal of Neuroscience

Cover image for Vol. 37 Issue 10

May 2013

Volume 37, Issue 10

Pages 1550–1725

  1. REVIEW

    1. Top of page
    2. REVIEW
    3. DEVELOPMENTAL NEUROSCIENCE
    4. MOLECULAR AND SYNAPTIC MECHANISMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Uncovering novel actors in astrocyte–neuron crosstalk in Parkinson's disease: the Wnt/β-catenin signaling cascade as the common final pathway for neuroprotection and self-repair (pages 1550–1563)

      Bianca Marchetti, Francesca L'Episcopo, Maria Concetta Morale, Cataldo Tirolo, Nuccio Testa, Salvo Caniglia, Maria Francesca Serapide and Stefano Pluchino

      Article first published online: 5 MAR 2013 | DOI: 10.1111/ejn.12166

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      In this review, the contribution of reactive astrocytes and their ability to modulate midbrain dopaminergic neurodegeneration, neuroprotection and neurorepair in MPTP rodent model of Parkinson's disease (PD) will be discussed in the light of novel emerging evidence implicating Wingless-type MMTV integration site (Wnt)/β-catenin signaling as a strong a candidate in MPTP-induced nigrostriatal dopaminergic plasticity, with implications for identifying new potential therapeutic targets in PD.

  2. DEVELOPMENTAL NEUROSCIENCE

    1. Top of page
    2. REVIEW
    3. DEVELOPMENTAL NEUROSCIENCE
    4. MOLECULAR AND SYNAPTIC MECHANISMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Prenatal ontogeny of the dopamine-dependent neurobehavioral phenotype in Pitx3-deficient mice (pages 1564–1572)

      Gale A. Kleven, Priyanka Joshi, Marco Voogd and April E. Ronca

      Article first published online: 13 MAR 2013 | DOI: 10.1111/ejn.12184

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      Across the last four days of gestation, Pitx3 mutants showed significantly increased latencies to exhibit Facial Wiping response to oral/tactile stimulation as compared to both heterozygous and C57BL/6J controls. These findings provide evidence that the primary fetal neurobehavioral deficit of the Pitx3 mutation is akinesia related to nigrostriatal damage. These results further demonstrate the sensitivity of fetal neurobehavioral assessments in the detection of emerging neural dysfunction, suggesting utility for prenatal diagnosis.

    2. Role of neuropilin-2 in the ipsilateral growth of midbrain dopaminergic axons (pages 1573–1583)

      Makio Torigoe, Kenta Yamauchi, Atsushi Tamada, Ikuo Matsuda, Atsu Aiba, Valérie Castellani and Fujio Murakami

      Article first published online: 27 MAR 2013 | DOI: 10.1111/ejn.12190

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      Axonal projections in the CNS are either crossed or uncrossed. Previous works indicated that Slits/Robos signaling controls the formation of uncrossed projections. Here we show that a mechanism mediated by Neuropilin-2 also regulates the formation of uncrossed projections of midbrain dopaminergic neurons. Interestingly, we found evidence that this mechanism is independent of Sema3s, major ligands for Neuropilin-2, and several other known guidance cues.

    3. Perturbations in cortical development and neuronal network excitability arising from prenatal exposure to benzodiazepines in mice (pages 1584–1593)

      Matilda Haas, Zhengdong Qu, Tae Hwan Kim, Ernesto Vargas, Kenneth Campbell, Steven Petrou, Seong-Seng Tan, Christopher A. Reid and Julian Heng

      Article first published online: 4 MAR 2013 | DOI: 10.1111/ejn.12167

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      The secreted neurotransmitter GABA has been proposed to influence the migratory behaviour and terminal differentiation of embryonic cortical neurons, but its long term effects on cortical development and adult brain function are unknown. In this study, we report that prenatal exposure to the GABAA receptor agonist diazepam results in long-lasting changes to the distribution of interneurons within the cortex, and alters the sensitivity of mice to a proconvulsant challenge. Our studies show that exposure of the fetal brain to benzodiazepines has consequences for the positioning of neurons and cortical network excitability.

    4. Development of cortical influences on superior colliculus multisensory neurons: effects of dark-rearing (pages 1594–1601)

      Liping Yu, Jinghong Xu, Benjamin A. Rowland and Barry E. Stein

      Article first published online: 27 MAR 2013 | DOI: 10.1111/ejn.12182

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      Rearing cats from birth to adulthood in darkness prevents neurons in the superior colliculus (SC) from developing the capability to integrate visual and non-visual (e.g. visual-auditory) inputs. Presumably, this developmental anomaly is due to a lack of experience with the combination of those cues, which is essential to form associative links between them.

    5. Social isolation perturbs experience-driven synaptic glutamate receptor subunit 4 delivery in the developing rat barrel cortex (pages 1602–1609)

      Tomoyuki Miyazaki, Misako Kunii, Susumu Jitsuki, Akane Sano, Yoshiyuki Kuroiwa and Takuya Takahashi

      Article first published online: 20 MAR 2013 | DOI: 10.1111/ejn.12188

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      We recently reported that early social isolation disrupts experience-driven GluA1 delivery to layer 4-2/3 pyramidal synapses during P12-14. Here, we report that neonatal isolation impacts even earlier stages of development by preventing experience-dependent synaptic GluA4 delivery. Thus, social isolation severely affects synaptic maturation throughout early postnatal development.

  3. MOLECULAR AND SYNAPTIC MECHANISMS

    1. Top of page
    2. REVIEW
    3. DEVELOPMENTAL NEUROSCIENCE
    4. MOLECULAR AND SYNAPTIC MECHANISMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Protein kinase C activation causes neurite retraction via cyclinD1 and p60-katanin increase in rat hippocampal neurons (pages 1610–1619)

      Sirin Korulu, Aysegul Yildiz-Unal, Meral Yuksel and Arzu Karabay

      Article first published online: 15 MAR 2013 | DOI: 10.1111/ejn.12185

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      We investigated the role of PKC on cyclinD1 regulation in hippocampal neurons and found that PKC activation increased nuclear cyclinD1 and PKC-α, but not PKC-ε. Moreover, nuclear PKC-α and cyclinD1 interfered with differentiation by promoting microtubule re-organisation via changing p60- katanin, p53 levels and phosphorylation status of tau and pRb. Relationship of the cell cycle in postmitotic neurons is a compelling irony that may have important roles in both development and differentiation.

    2. The delta subfamily of glutamate receptors: characterization of receptor chimeras and mutants (pages 1620–1630)

      Angela Orth, Daniel Tapken and Michael Hollmann

      Article first published online: 31 MAR 2013 | DOI: 10.1111/ejn.12193

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      Based on sequence homology, the delta receptors, GluD1 and GluD2, are regarded as a subfamily of the ionotropic glutamate receptors (iGluRs). However, they have not been shown to respond to glutamatergic agonists. We demonstrate that both delta receptors have functional gating machineries and ion permeation pathways similar but not identical to those of other iGluRs. The key differences between delta receptors and other iGluRs appear to be located within the ligand binding domain.

    3. A role for vesicular glutamate transporter 1 in synaptic vesicle clustering and mobility (pages 1631–1642)

      Léa Siksou, Kätlin Silm, Christoph Biesemann, Ralf B. Nehring, Sonja M. Wojcik, Antoine Triller, Salah El Mestikawy, Serge Marty and Etienne Herzog

      Article first published online: 15 APR 2013 | DOI: 10.1111/ejn.12199

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      Synaptic vesicles (SVs) from excitatory synapses carry Vesicular GLUtamate Transporters (VGLUTs) that fill the vesicles with neurotransmitter. We demonstrate that the tubular structures previously described in presynaptic terminals of VGLUT1 KO mice were due to a flattening of SVs induced by the aldehyde fixation, indicating that VGLUT1 increases the tonicity of SVs. Also, the reduced number of SVs in presynaptic terminals is paralleled by an increased trafficking of SVs in intersynaptic axonal segments in the VGLUT1 KO, pointing for a new role of VGLUT1 in vesicles clustering.

    4. Increased hippocampal NgR1 signaling machinery in aged rats with deficits of spatial cognition (pages 1643–1658)

      Heather D. VanGuilder Starkey, William E. Sonntag and Willard M. Freeman

      Article first published online: 26 FEB 2013 | DOI: 10.1111/ejn.12165

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      Hippocampal expression of NgR1 co-receptors (LINGO-1, p75, TROY) is upregulated in a rodent model of age-related cognitive decline and correlates significantly with spatial learning and memory ability. NgR1 and NgR1 co-receptors are co-expressed by hippocampal neurons in aged cognitively impaired rats, and NgR1 pathway component expression accurately classifies rats by cognitive status. These data suggest that signaling through NgR1 co-receptors may play a causative role in cognitive decline.

    5. Quantitative and ultrastructural study of serotonin innervation of the globus pallidus in squirrel monkeys (pages 1659–1668)

      Lara Eid, Marie-France Champigny, André Parent and Martin Parent

      Article first published online: 25 FEB 2013 | DOI: 10.1111/ejn.12164

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      Unbiased examination of 5-HT axon varicosities in GPi and GPe of squirrel monkey indicates a decreasing anteroposterior gradient. Less than 25% of 5-HT varicosities display a synaptic contact, exclusively found on pallidal dendrites, indicating that 5-HT exerts its modulatory effect upon pallidal afferents mainly through diffuse transmission, whereas its direct control of pallidal neurons results from both synaptic and diffuse transmission.

  4. DISORDERS OF THE NERVOUS SYSTEM

    1. Top of page
    2. REVIEW
    3. DEVELOPMENTAL NEUROSCIENCE
    4. MOLECULAR AND SYNAPTIC MECHANISMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. A dietary polyphenol resveratrol acts to provide neuroprotection in recurrent stroke models by regulating AMPK and SIRT1 signaling, thereby reducing energy requirements during ischemia (pages 1669–1681)

      Li-Mei Wang, Yong-Jiu Wang, Min Cui, Wen-Juan Luo, Xiao-Ji Wang, Philip A. Barber and Zhe-Yu Chen

      Article first published online: 5 MAR 2013 | DOI: 10.1111/ejn.12162

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      Resveratrol (RSV) administration significantly reduced infarct volumes, improved behavioral, increased AMPK and SIRT1activities and decreased energy assumption and restored cell energy ATP level in recurrent ischemic stroke models. RSV provides neuroprotection in recurrent stroke models by regulating the AMPK and SIRT1 signaling thereby reducing energy requirements during ischemia.

    2. Lack of galectin-3 speeds Wallerian degeneration by altering TLR and pro-inflammatory cytokine expressions in injured sciatic nerve (pages 1682–1690)

      Bruno Siqueira Mietto, Sofia Jurgensen, Lucinéia Alves, Cyntia Pecli, Marcelo Sampaio Narciso, Iranaia Assunção-Miranda, Dea Maria Serra Villa-Verde, Flávia Regina de Souza Lima, João Ricardo Lacerda de Menezes, Cláudia Farias Benjamim, Marcelo Torres Bozza and Ana Maria Blanco Martinez

      Article first published online: 14 FEB 2013 | DOI: 10.1111/ejn.12161

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      The lack of Gal-3 after sciatic nerve injury speeds Wallerian degeneration (WD) by augmenting the inflammatory profile of WD and by accelerating myelin breakdown and clearance. In addition, the absence of Gal-3 in macrophages and Schwann cells results in an improvement in their phagocytic potential.

    3. Behavioural recovery on simple and complex tasks by means of cell replacement therapy in unilateral 6-hydroxydopamine-lesioned mice (pages 1691–1704)

      Andreas Heuer, Ngoc-Nga Vinh and Stephen B. Dunnett

      Article first published online: 25 FEB 2013 | DOI: 10.1111/ejn.12150

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      Unilateral 6-hydroxydopamine lesions to the medial forebrain bundle cause impairments on simple behavioural tests and the lateralised choice reaction time task conducted in the 9-hole operant box. Dopamine-rich primary fetal tissue grafts were able to ameliorate the lesion-induced deficits on some but not all parameters. The behavioural tests presented are useful drug-free approaches for evaluating cell based therapies.

    4. Role of a novel nociceptor autocrine mechanism in chronic pain (pages 1705–1713)

      Luiz F. Ferrari, Emma Levine and Jon D. Levine

      Article first published online: 4 FEB 2013 | DOI: 10.1111/ejn.12145

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      Intradermal injection of PGE2 induces a PKA-dependent short-term hyperalgesia. However, in a model of chronic pain, hyperalgesic priming, produced by a previous inflammatory stimulus, PGE2 hyperalgesia is prolonged; in addition to PKA, there is now a late, PKCε-dependent, component. We provide evidence that the extracellular cAMP-adenosine pathway, in the peripheral terminal of the nociceptor, is the underlying mechanism for the delayed PKCε-dependent hyperalgesia.

    5. γ-Secretase binding sites in aged and Alzheimer's disease human cerebrum: the choroid plexus as a putative origin of CSF Aβ (pages 1714–1725)

      Fei Liu, Zhi-Qin Xue, Si-Hao Deng, Xiong Kun, Xue-Gang Luo, Peter R. Patrylo, Gregory M. Rose, Huaibin Cai, Robert G. Struble, Yan Cai and Xiao-Xin Yan

      Article first published online: 22 FEB 2013 | DOI: 10.1111/ejn.12159

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      Deposition of β -amyloid (Aβ) peptides, cleavage products of β-amyloid precursor protein (APP) by β-secretase-1 (BACE1) and γ-secretase, is a neuropathological hallmark of Alzheimer's disease (AD). γ-Secretase inhibition is a therapeutic anti-Aβ approach, although it is unclear whether the enzyme's activity is altered in AD brain.

      Corrected by:

      Corrigendum: γ-Secretase binding sites in aged and Alzheimer's disease human cerebrum: the choroid plexus as a putative origin of CSF Aβ

      Vol. 38, Issue 2, 2340, Article first published online: 14 JUL 2013

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