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Cntnap4 differentially contributes to GABAergic and dopaminergic synaptic transmission

Author

Listed:
  • T. Karayannis

    (NYU Neuroscience Institute)

  • E. Au

    (NYU Neuroscience Institute)

  • J. C. Patel

    (Neuroscience and Physiology, New York University Langone Medical Center)

  • I. Kruglikov

    (NYU Neuroscience Institute)

  • S. Markx

    (College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, New York 10032, USA)

  • R. Delorme

    (Institut Pasteur, Human Genetics and Cognitive Functions Unit, 75724 Paris, France
    CNRS URA 2182 Genes, Synapses and Cognition, Institut Pasteur, 75724 Paris, France
    Assistance Publique-Hôpitaux de Paris, Robert Debré Hospital, 75019 Paris, France)

  • D. Héron

    (Unité Fonctionnelle de Génétique Médicale AP-HP, Centre de Référence, Déficiences intellectuelles de causes rares, CRicm, UMR-S975, Groupe Hospitalier Pitié-Salpêtrière, F-75013, Paris, France)

  • D. Salomon

    (Weizmann Institute of Science, Rehovot 76100, Israel)

  • J. Glessner

    (Center for Applied Genomics, The Children’s Hospital of Philadelphia)

  • S. Restituito

    (NYU Neuroscience Institute)

  • A. Gordon

    (Weizmann Institute of Science, Rehovot 76100, Israel)

  • L. Rodriguez-Murillo

    (College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, New York 10032, USA)

  • N. C. Roy

    (NYU Neuroscience Institute
    Section on Synaptic Transmission, National Institute on Deafness and Other Communication Disorders, National Institutes of Health)

  • J. A. Gogos

    (Columbia University Medical Center)

  • B. Rudy

    (NYU Neuroscience Institute)

  • M. E. Rice

    (Neuroscience and Physiology, New York University Langone Medical Center)

  • M. Karayiorgou

    (College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, New York 10032, USA)

  • H. Hakonarson

    (Institut Pasteur, Human Genetics and Cognitive Functions Unit, 75724 Paris, France)

  • B. Keren

    (Unité Fonctionnelle de Génétique Chromosomique AP-HP, CRicm, UMR-S975, Groupe Hospitalier, Pitié-Salpêtrière, 75013 Paris, France)

  • G. Huguet

    (Institut Pasteur, Human Genetics and Cognitive Functions Unit, 75724 Paris, France
    CNRS URA 2182 Genes, Synapses and Cognition, Institut Pasteur, 75724 Paris, France
    University Paris Diderot, Sorbonne Paris Cité, Human Genetics and Cognitive Functions, 75005 Paris, France)

  • T. Bourgeron

    (Institut Pasteur, Human Genetics and Cognitive Functions Unit, 75724 Paris, France
    CNRS URA 2182 Genes, Synapses and Cognition, Institut Pasteur, 75724 Paris, France
    University Paris Diderot, Sorbonne Paris Cité, Human Genetics and Cognitive Functions, 75005 Paris, France
    FondaMental Foundation, 94000 Créteil, France)

  • C. Hoeffer

    (NYU Neuroscience Institute)

  • R. W. Tsien

    (NYU Neuroscience Institute)

  • E. Peles

    (Weizmann Institute of Science, Rehovot 76100, Israel)

  • G. Fishell

    (NYU Neuroscience Institute)

Abstract

The molecular relationship between synaptic dysfunction and psychiatric disorders was investigated using a mouse model system; presynaptically localized Cntnap4 is required for the output of two disease-relevant neuronal subpopulations (cortical parvalbumin-positive GABAergic cells and midbrain dopaminergic neurons) and Cntnap4 mutants show behavioural abnormalities which can be pharmacologically reversed.

Suggested Citation

  • T. Karayannis & E. Au & J. C. Patel & I. Kruglikov & S. Markx & R. Delorme & D. Héron & D. Salomon & J. Glessner & S. Restituito & A. Gordon & L. Rodriguez-Murillo & N. C. Roy & J. A. Gogos & B. Rudy , 2014. "Cntnap4 differentially contributes to GABAergic and dopaminergic synaptic transmission," Nature, Nature, vol. 511(7508), pages 236-240, July.
    • Handle: RePEc:nat:nature:v:511:y:2014:i:7508:d:10.1038_nature13248
    DOI: 10.1038/nature13248
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    Cited by:

    1. Lauren Rylaarsdam & Jennifer Rakotomamonjy & Eleanor Pope & Alicia Guemez-Gamboa, 2024. "iPSC-derived models of PACS1 syndrome reveal transcriptional and functional deficits in neuron activity," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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