European Journal of Neuroscience

Cover image for Vol. 39 Issue 7

Special Issue: SYNAPTIC BASIS OF DISEASE

April 2014

Volume 39, Issue 7

Pages 1057–1244

  1. SPECIAL ISSUE: SYNAPTIC BASIS OF DISEASE

    1. Top of page
    2. SPECIAL ISSUE: SYNAPTIC BASIS OF DISEASE
    3. Special Issue Technical Spotlight
    1. You have free access to this content
      The synaptic basis of disease (pages 1057–1058)

      Scott Thompson and Christian Luscher

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12560

    2. The synapse in schizophrenia (pages 1059–1067)

      Andrew J. Pocklington, Michael O'Donovan and Michael J. Owen

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12489

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      It is several decades since synaptic dysfunction was first suggested to play a role in schizophrenia. We outline current understanding of the genetic architecture of schizophrenia and examine the evidence for synaptic involvement. A strong case can now be made that disruption of glutamatergic signalling pathways regulating synaptic plasticity contributes to the aetiology of schizophrenia.

    3. You have full text access to this OnlineOpen article
      Disrupted in schizophrenia 1 and synaptic function in the mammalian central nervous system (pages 1068–1073)

      Andrew D. Randall, Mai Kurihara, Nicholas J. Brandon and Jon T. Brown

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12500

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      The DISC1 gene is found at the breakpoint of an inherited chromosomal translocation, and segregates with major mental illnesses. The product of this gene (the DISC1 protein) is found in multiple CNS cell types where it works in concert with a range of binding partners to contribute to multiple aspects of CNS biology, including both pre- and postsynaptic function.

    4. You have full text access to this OnlineOpen article
      Neurophysiological modification of CA1 pyramidal neurons in a transgenic mouse expressing a truncated form of disrupted-in-schizophrenia 1 (pages 1074–1090)

      Clair A. Booth, Jonathan T. Brown and Andrew D. Randall

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12549

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      A t(1;11) balanced chromosomal translocation transects the Disc1 gene in a large Scottish family and produces genome-wide linkage to schizophrenia and recurrent major depressive disorder. This study describes our in vitro investigations into neurophysiological function in hippocampal area CA1 of a transgenic mouse (DISC1tr) that expresses a truncated version of DISC1 designed to reproduce aspects of the genetic situation in the Scottish t(1;11) pedigree.

    5. You have free access to this content
      Neural oscillations during non-rapid eye movement sleep as biomarkers of circuit dysfunction in schizophrenia (pages 1091–1106)

      Richard J. Gardner, Flavie Kersanté, Matthew W. Jones and Ullrich Bartsch

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12533

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      The neurophysiology of non-rapid eye movement sleep is characterized by the occurrence of neural network oscillations with distinct origins and frequencies, which act in concert to support sleep-dependent information processing. Thalamocortical circuits generate slow (0.1–4 Hz) oscillations reflecting synchronized temporal windows of cortical activity, whilst concurrent waxing-waning spindle oscillations (8–15 Hz) act to facilitate cortical plasticity.

    6. Heterogeneity and convergence: the synaptic pathophysiology of autism (pages 1107–1113)

      Stéphane J. Baudouin

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12498

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      Autism is a developmental disorder characterised by a high heterogeneity of clinical diagnoses and genetic associations. This heterogeneity is a challenge for the identification of the pathophysiology of the disease and for the development of new therapeutic strategies.

    7. Synaptic basis of social dysfunction: a focus on postsynaptic proteins linking group-I mGluRs with AMPARs and NMDARs (pages 1114–1129)

      Eoin C. O'Connor, Sebastiano Bariselli and Camilla Bellone

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12510

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      Most of us engage in social interactions on a daily basis and the repertoire of social behaviors we acquire during development and later in life are incredibly varied. However, in many neurodevelopmental disorders, including Autism Spectrum Disorders (ASDs), social behavior is severely compromised and indeed this represents a key diagnostic component for such conditions.

    8. Reversal of activity-mediated spine dynamics and learning impairment in a mouse model of Fragile X syndrome (pages 1130–1137)

      Bernadett Boda, Pablo Mendez, Benjamin Boury-Jamot, Fulvio Magara and Dominique Muller

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12488

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      Fragile X syndrome (FXS) is characterized by intellectual disability and autistic traits and results from the silencing of the FMR1 gene coding for a protein implicated in the regulation of protein synthesis at synapses. The lack of functional FMRP protein has been proposed to result in an excessive signaling of synaptic metabotropic glutamate receptors, leading to alterations of synapse maturation and plasticity.

    9. Auxiliary proteins promote modal gating of AMPA- and kainate-type glutamate receptors (pages 1138–1147)

      Wei Zhang, Suma Priya Sudarsana Devi, Susumu Tomita and James R. Howe

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12519

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      Association of either AMPA or kainate receptors with auxiliary subunits results in the appearance of a slow component in the decay of ensemble responses to rapid applications of saturating concentrations of glutamate. We show here that these components arise from distinct gating behaviors, which we refer to as modes because individual receptors switch between low- and high-Popen gating on a time-scale of seconds. The presence of receptors displaying both types of gating has a large impact on both the kinetics and amplitude of ensemble currents similar to those seen at synapses.

    10. Casein kinase 2 phosphorylates GluA1 and regulates its surface expression (pages 1148–1158)

      Marc P. Lussier, Xinglong Gu, Wei Lu and Katherine W. Roche

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12494

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      Many studies demonstrate that the phosphorylation of AMPARs regulates receptor trafficking and function. Our findings now show that the loop1 region of GluA1 is phosphorylated in vitro by several kinases. Specifically, CK2 phosphorylates GluA1 serine 579, which regulates synaptic targeting and modulates basal synaptic transmission in neurons. Our results thus demonstrate a molecular pathway underlying the action of CK2 at excitatory synapses and reveal a novel mechanism for regulating AMPARs.

    11. BDNF contributes to both rapid and homeostatic alterations in AMPA receptor surface expression in nucleus accumbens medium spiny neurons (pages 1159–1169)

      Jeremy M. Reimers, Jessica A. Loweth and Marina E. Wolf

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12422

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      In cultured medium spiny neurons of the nucleus accumbens, acute BDNF (30 min) increases AMPAR surface expression via ERK activation, while longer BDNF incubation (24 h) reduces AMPAR surface expression. BDNF-TrkB signaling is required for homeostatic reductions in AMPAR surface expression (scaling down) in response to a prolonged increase in excitatory transmission. These bidirectional effects of BDNF may help explain its role in cocaine-induced neuroadaptations in the nucleus accumbens.

    12. The lateral habenula in addiction and depression: an anatomical, synaptic and behavioral overview (pages 1170–1178)

      Salvatore Lecca, Frank J. Meye and Manuel Mameli

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12480

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      Our current understanding of the function of lateral habenula (LHb) neurons in the context of reward, aversion and related pathologies is largely based on anatomical and lesioning studies. Only very recently the function, and implications of this structure in motivational states, as well as its cellular and synaptic adaptations in physiology as well as in depressive-like state and after drug exposure gained a large attention. This has made the LHb an ideal model to dissect the causal relationship between cellular plasticity and behavioral outcome in the pathophysiology of motivation.

    13. You have free access to this content
      Stress and VTA synapses: implications for addiction and depression (pages 1179–1188)

      Abigail M. Polter and Julie A. Kauer

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12490

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      While stressful experiences are a part of everyone's life, they can also exact a major toll on health. Stressful life experiences are associated with increased substance abuse, and there exists significant co-morbidity between mental illness and substance use disorders (Volkow & Li, 2004; Koob & Kreek, 2007; Sinha, 2008).

    14. Interplay between synaptic endocannabinoid signaling and metaplasticity in neuronal circuit function and dysfunction (pages 1189–1201)

      Miriam Melis, Barbara Greco and Raffaella Tonini

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12501

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      Neuromodulation acts across different functional domains to regulate dynamic synaptic changes and behavior. Here, we reviewed past and recent evidence for endocannabinoid-mediated modulation of synaptic plasticity by inferring that interconnected functional activation states of eCB signaling (prior, tonic and persistent) may contribute to metaplastic control of synaptic and behavioral functions in health and disease.

    15. Tau acts as a mediator for Alzheimer's disease-related synaptic deficits (pages 1202–1213)

      Dezhi Liao, Eric C. Miller and Peter J. Teravskis

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12504

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      The two histopathological hallmarks of Alzheimer's disease (AD) are amyloid plaques containing multiple forms of Aβ and neurofibrillary tangles containing phosphorylated tau proteins. Our recent live imaging studies clearly show that both changes in Aβ and tau can induce tau mislocalization to dendritic spines, illustrating a part of the multiple signaling pathways for AD pathogenesis.

    16. Tau phosphorylation and tau mislocalization mediate soluble Aβ oligomer-induced AMPA glutamate receptor signaling deficits (pages 1214–1224)

      Eric C. Miller, Peter J. Teravskis, Benjamin W. Dummer, Xiaohui Zhao, Richard L. Huganir and Dezhi Liao

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12507

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      In our previous studies, phosphorylation dependent tau mislocalization to dendritic spines resulted in early cognitive and synaptic deficits. In this study, we present a new aspect of Alzheimer's disease pathogenesis: changes in APP or Amyloid beta can cause tau mislocalization and tau-mediated synaptic deficits.

    17. Synapto-depressive effects of amyloid beta require PICK1 (pages 1225–1233)

      Stephanie Alfonso, Helmut W. Kessels, Charles C. Banos, Timothy R. Chan, Edward T. Lin, Gnanasambandam Kumaravel, Robert H. Scannevin, Kenneth J. Rhodes, Richard Huganir, Kevin M. Guckian, Anthone W. Dunah and Roberto Malinow

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12499

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      Aβ reduces synaptic and surface GluA2-containing AMPA-Rs in wild-type but not PICK1-/- tissue. A synthetic compound blocking GluA2-PICK1 interactions blocks effects of Aβ. These data are consistent with a model in which Aβ drives signaling leading to intracellular retention of GluA2-containing AMPA-Rs by PICK1.

  2. Special Issue Technical Spotlight

    1. Top of page
    2. SPECIAL ISSUE: SYNAPTIC BASIS OF DISEASE
    3. Special Issue Technical Spotlight
    1. Fluorescence-activated sorting of fixed nuclei: a general method for studying nuclei from specific cell populations that preserves post-translational modifications (pages 1234–1244)

      Lucile Marion-Poll, Enrica Montalban, Annie Munier, Denis Hervé and Jean-Antoine Girault

      Version of Record online: 8 APR 2014 | DOI: 10.1111/ejn.12506

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      FAST-FIN is a rapid and efficient method for isolating cell type-specific nuclei from fixed brain. It allows the preservation and study of labile post-translational protein modifications.

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