IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v3y2012i1d10.1038_ncomms2295.html
   My bibliography  Save this article

Rapamycin reverses impaired social interaction in mouse models of tuberous sclerosis complex

Author

Listed:
  • Atsushi Sato

    (Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science
    Graduate School of Medicine, The University of Tokyo
    Graduate School of Medicine, The University of Tokyo)

  • Shinya Kasai

    (Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science)

  • Toshiyuki Kobayashi

    (Graduate School of Medicine, Juntendo University)

  • Yukio Takamatsu

    (Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science)

  • Okio Hino

    (Graduate School of Medicine, Juntendo University)

  • Kazutaka Ikeda

    (Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science)

  • Masashi Mizuguchi

    (Graduate School of Medicine, The University of Tokyo)

Abstract

Impairment of reciprocal social interaction is a core symptom of autism spectrum disorder. Genetic disorders frequently accompany autism spectrum disorder, such as tuberous sclerosis complex caused by haploinsufficiency of the TSC1 and TSC2 genes. Accumulating evidence implicates a relationship between autism spectrum disorder and signal transduction that involves tuberous sclerosis complex 1, tuberous sclerosis complex 2 and mammalian target of rapamycin. Here we show behavioural abnormalities relevant to autism spectrum disorder and their recovery by the mammalian target of rapamycin inhibitor rapamycin in mouse models of tuberous sclerosis complex. In Tsc2+/− mice, we find enhanced transcription of multiple genes involved in mammalian target of rapamycin signalling, which is dependent on activated mammalian target of rapamycin signalling with a minimal influence of Akt. The findings indicate a crucial role of mammalian target of rapamycin signalling in deficient social behaviour in mouse models of tuberous sclerosis complex, supporting the notion that mammalian target of rapamycin inhibitors may be useful for the pharmacological treatment of autism spectrum disorder associated with tuberous sclerosis complex and other conditions that result from dysregulated mammalian target of rapamycin signalling.

Suggested Citation

  • Atsushi Sato & Shinya Kasai & Toshiyuki Kobayashi & Yukio Takamatsu & Okio Hino & Kazutaka Ikeda & Masashi Mizuguchi, 2012. "Rapamycin reverses impaired social interaction in mouse models of tuberous sclerosis complex," Nature Communications, Nature, vol. 3(1), pages 1-9, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2295
    DOI: 10.1038/ncomms2295
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms2295
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms2295?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Vasiliki Karalis & Franklin Caval-Holme & Helen S. Bateup, 2022. "Raptor downregulation rescues neuronal phenotypes in mouse models of Tuberous Sclerosis Complex," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    2. Marco Pagani & Noemi Barsotti & Alice Bertero & Stavros Trakoshis & Laura Ulysse & Andrea Locarno & Ieva Miseviciute & Alessia De Felice & Carola Canella & Kaustubh Supekar & Alberto Galbusera & Vinod, 2021. "mTOR-related synaptic pathology causes autism spectrum disorder-associated functional hyperconnectivity," Nature Communications, Nature, vol. 12(1), pages 1-15, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2295. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.