European Journal of Neuroscience

Cover image for Vol. 38 Issue 1

July 2013

Volume 38, Issue 1

Pages 2019–2198

  1. REVIEW

    1. Top of page
    2. REVIEW
    3. MOLECULAR AND SYNAPTIC MECHANISMS
    4. NEUROSYSTEMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Cellular and molecular mechanisms controlling the migration of neocortical interneurons (pages 2019–2029)

      Oscar Marín

      Article first published online: 8 MAY 2013 | DOI: 10.1111/ejn.12225

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      The goal of the present review is to discuss our current understanding of the cellular and molecular mechanisms controlling the migration of cortical GABAergic interneurons, with an emphasis on those migrating to the neocortex. The data summarized here demonstrate that different mechanisms operate at distinct phases in the migration of interneurons from the subpallium to their final destination in the neocortex.

  2. MOLECULAR AND SYNAPTIC MECHANISMS

    1. Top of page
    2. REVIEW
    3. MOLECULAR AND SYNAPTIC MECHANISMS
    4. NEUROSYSTEMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Rare contacts between synapses and microglial processes containing high levels of Iba1 and actin – a postembedding immunogold study in the healthy rat brain (pages 2030–2040)

      Carl J. L. Sogn, Maja Puchades and Vidar Gundersen

      Article first published online: 17 APR 2013 | DOI: 10.1111/ejn.12213

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      In order to influence synaptic communication microglia move in the neuropil and contact synapses. By immunogold electron microscopy we here show that at a given time point direct interaction between microglia and synapses in the brain is rather infrequent. However, the most delicate microglial processes, which are the ones that contact synapses, are equipped with high levels of Iba1 and actin, enabling them to move in the neuropil.

    2. Differential molecular profiles of astrocytes in degeneration and re-innervation after sensory deafferentation of the adult rat cochlear nucleus (pages 2041–2056)

      Michaela Fredrich, Anne C. Zeber, Heika Hildebrandt and Robert-Benjamin Illing

      Article first published online: 15 APR 2013 | DOI: 10.1111/ejn.12200

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      Ablating the cochlea of adult rats causes a total sensory deafferentation of the cochlear nucleus. Degeneration of the auditory nerve and its synaptic terminals temporally overlaps with the formation of new synapses in the cochlear nucleus. We show that the process of establishing new synaptic contacts prompts astrocytes to recompose their molecular profile, indicating that they are an integral component of a lesion-induced re-organisation in the adult brain.

    3. NOMPC is likely a key component of Drosophila mechanotransduction channels (pages 2057–2064)

      Jiaxin Gong, Qingxiu Wang and Zuoren Wang

      Article first published online: 17 APR 2013 | DOI: 10.1111/ejn.12214

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      In this work, we studied the roles of Drosophila NOMPC in mechanotransduction. Here we report our findings that the previously reported NOMPC-dependent adapting mechanoreceptor current (MRC) responses in external bristle mechanosensory organs are chloride-dependent, and NOMPC is likely a key component of Drosophila mechanotransduction channels. These findings provide important clues toward understanding the mechanism of mechanosensation in the fruit fly.

  3. NEUROSYSTEMS

    1. Top of page
    2. REVIEW
    3. MOLECULAR AND SYNAPTIC MECHANISMS
    4. NEUROSYSTEMS
    5. DISORDERS OF THE NERVOUS SYSTEM
    1. Fluoxetine and serotonin facilitate attractive-adaptation-induced orientation plasticity in adult cat visual cortex (pages 2065–2077)

      Lyes Bachatene, Vishal Bharmauria, Sarah Cattan and Stéphane Molotchnikoff

      Article first published online: 15 APR 2013 | DOI: 10.1111/ejn.12206

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      Fluoxetine is a widely prescribed drug which is well known for its antidepressant activity by selective inhibition of recapture of serotonin in the brain. Using orientation tuning curve shifts as a model, we show that fluoxetine and serotonin facilitate attractive-adaptation-induced-orientation short-term plasticity in the primary visual cortex without modulating the firing rate of neurons.

    2. Methamphetamine-induced neurotoxicity disrupts naturally occurring phasic dopamine signaling (pages 2078–2088)

      Christopher D. Howard, David P. Daberkow, Eric S. Ramsson, Kristen A. Keefe and Paul A. Garris

      Article first published online: 11 APR 2013 | DOI: 10.1111/ejn.12209

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      Methamphetamine (METH) neurotoxicity leads to long-term damage to brain dopamine (DA) systems. Here we demonstrate that METH-induced DA depletion causes deficits in phasic DA signaling, which is important to reward-based learning, in freely-moving rats. This is the first report identifying deficits in naturally occurring phasic DA signaling in any DA-denervation model, and these deficits may serve as a mechanistic link between DA depletion and cognitive impairments associated with METH abuse.

    3. Early-life stress affects the structural and functional plasticity of the medial prefrontal cortex in adolescent rats (pages 2089–2107)

      Agnieszka Chocyk, Bartosz Bobula, Dorota Dudys, Aleksandra Przyborowska, Iwona Majcher-Maślanka, Grzegorz Hess and Krzysztof Wędzony

      Article first published online: 15 APR 2013 | DOI: 10.1111/ejn.12208

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      Early life experiences are crucial factors that shape brain development and function due to their ability to induce structural and functional plasticity. Among these experiences, early life stress (ELS) is known to interfere with brain development and maturation, increasing the risk of future psychopathologies, including depression, anxiety, and personality disorders.

    4. Feedback and feedforward adaptation to visuomotor delay during reaching and slicing movements (pages 2108–2123)

      Lior Botzer and Amir Karniel

      Article first published online: 22 MAY 2013 | DOI: 10.1111/ejn.12211

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      We investigated the control of reaching movements during an imposed visuomotor delay. In a series of two experiments, subjects learned to reach and to perform rhythmic movements using a visual feedback cue to a spatial target. Our findings show that subjects can adapt to visual delay, and our computational model and simulations explain these results based on two adapted forward models and a third feedforward controller, while refuting delay representation in a pure forward vision-based predictor.

  4. DISORDERS OF THE NERVOUS SYSTEM

    1. Top of page
    2. REVIEW
    3. MOLECULAR AND SYNAPTIC MECHANISMS
    4. NEUROSYSTEMS
    5. DISORDERS OF THE NERVOUS SYSTEM
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    2. Featured Article
      Atypical cortical representation of peripheral visual space in children with an autism spectrum disorder (pages 2125–2138)

      Hans-Peter Frey, Sophie Molholm, Edmund C. Lalor, Natalie N. Russo and John J. Foxe

      Article first published online: 21 MAY 2013 | DOI: 10.1111/ejn.12243

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      A key feature of early visual cortical regions is that they contain discretely organized retinotopic maps. Titration of these maps must occur through experience, and the fidelity of their spatial tuning will depend on the consistency and accuracy of the eye-movement system.

    3. Transcriptome profiling of hippocampal CA1 after early-life seizure-induced preconditioning may elucidate new genetic therapies for epilepsy (pages 2139–2152)

      L. K. Friedman, J. Mancuso, A. Patel, V. Kudur, J. R. Leheste, S. Iacobas, J. Botta, D. A. Iacobas and D. C. Spray

      Article first published online: 4 APR 2013 | DOI: 10.1111/ejn.12168

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      Injury of the CA1 subregion induced by a single injection of kainic acid (1×KA) is attenuated when juvenile animals (P20) have a history of two sustained neonatal seizures on P6 and P9. To identify gene candidates involved in the spatially protective effects produced by early life conditioning seizures we profiled and compared the transcriptomes of CA1 subregions from control, 1×KA, and 3×KA treated animals.

    4. Myelin loss and oligodendrocyte pathology in white matter tracts following traumatic brain injury in the rat (pages 2153–2165)

      J. Flygt, A. Djupsjö, F. Lenne and N. Marklund

      Article first published online: 5 MAR 2013 | DOI: 10.1111/ejn.12179

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      White matter injury is common following traumatic brain injury and may lead to reduced functional connectivity and impaired cognitive function. In two widely used models of traumatic brain injury, axonal injury, demyelination, oligodendrocyte death and oligodendrocyte precursor changes were evaluated. Brain injury caused widespread demyelination and axon injury, accompanied by apoptotic oligodendrocytes and an increased number of oligodendrocyte progenitors in white matter tracts.

    5. Cerebellum-dependent associative learning deficits in primary dystonia are normalized by rTMS and practice (pages 2166–2171)

      B. S. Hoffland, P. Kassavetis, M. Bologna, J. T. H. Teo, K. P. Bhatia, J. C. Rothwell, M. J. Edwards and B. P. van de Warrenburg

      Article first published online: 31 MAR 2013 | DOI: 10.1111/ejn.12186

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      Eyeblink classical conditioning (EBCC) is a cerebellum-dependent paradigm of associative motor learning and abnormal EBCC is a neurophysiological indicator of cerebellar dysfunction. We have previously demonstrated impaired EBCC in patients with primary dystonia, but it remains uncertain if this represents actual cerebellar pathology or reflects a functional cerebellar disruption.

    6. Striatal glutamate induces retrograde excitotoxicity and neuronal degeneration of intralaminar thalamic nuclei: their potential relevance for Parkinson's disease (pages 2172–2182)

      Ingrid Morales, Magdalena Sabate and Manuel Rodriguez

      Article first published online: 8 APR 2013 | DOI: 10.1111/ejn.12205

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      The striatal decrease of dopamine increased the extracelular glutamate pool. The glutamatergic thalamo-striatal pathway degenerated with the striatal increase of glutamate. Present data in rats suggest that glutamatergic hyperactivity in the striatum could be the cause of a retrograde degeneration of the intralaminar thalamic nuclei in Parkinson's disease.

    7. Deep brain stimulation of the subthalamic nucleus reverses oral tremor in pharmacological models of parkinsonism: interaction with the effects of adenosine A2A antagonism (pages 2183–2191)

      Lyndsey E. Collins-Praino, Nicholas E. Paul, Felicia Ledgard, Samantha J. Podurgiel, Rotem Kovner, Younis Baqi, Christa E. Müller, Patrick B. Senatus and John D. Salamone

      Article first published online: 18 APR 2013 | DOI: 10.1111/ejn.12212

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      The tremulous jaw movement (TJM) model was used to study the effects of subthalamic (STN) deep brain stimulation (DBS) in rats. STN DBS reduced the TJMs induced by dopamine antagonists and cholinomimetic drugs. The ability of DBS to suppress TJMs was dependent upon the neuroanatomical locus being stimulated, and the frequency and intensity of stimulation used. Administration of the adenosine A2A receptor antagonist MSX-3 reduced the frequency and intensity parameters needed to reduce TJMs.

    8. Haloperidol-induced striatal Nur77 expression in a non-human primate model of tardive dyskinesia (pages 2192–2198)

      Souha Mahmoudi, Pierre J. Blanchet and Daniel Lévesque

      Article first published online: 31 MAR 2013 | DOI: 10.1111/ejn.12198

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      Tardive dyskinesia (TD) is a delayed and potentially irreversible motor complication arising in patients chronically exposed to antipsychotic drugs. As several modern (so-called atypical) antipsychotic drugs are common offenders, the widening clinical indications for prescription as well as exposure of vulnerable individuals, TD will remain a significant drug-induced unwanted side effect.

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