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Hypothalamic proteoglycan syndecan-3 is a novel cocaine addiction resilience factor

Author

Listed:
  • Jihuan Chen

    (The Scripps Research Institute)

  • Vez Repunte-Canonigo

    (The Scripps Research Institute)

  • Tomoya Kawamura

    (The Scripps Research Institute)

  • Celine Lefebvre

    (Center for Computational Biology and Bioinformatics, Columbia University)

  • William Shin

    (Center for Computational Biology and Bioinformatics, Columbia University
    Columbia University)

  • Leonard L. Howell

    (Yerkes National Primate Research Center, Emory University)

  • Scott E. Hemby

    (Wake Forest School of Medicine)

  • Brandon K. Harvey

    (National Institute on Drug Abuse, Intramural Research Program, Neuronal Networks Section)

  • Andrea Califano

    (Center for Computational Biology and Bioinformatics, Columbia University
    Columbia University
    Columbia University
    Herbert Irving Comprehensive Cancer Center, Columbia University)

  • Marisela Morales

    (National Institute on Drug Abuse, Intramural Research Program, Neuronal Networks Section)

  • George F. Koob

    (Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute)

  • Pietro Paolo Sanna

    (The Scripps Research Institute)

Abstract

Proteoglycans like syndecan-3 have complex signaling roles in addition to their function as structural components of the extracellular matrix. Here, we show that syndecan-3 in the lateral hypothalamus has an unexpected new role in limiting compulsive cocaine intake. In particular, we observe that syndecan-3 null mice self-administer greater amounts of cocaine than wild-type mice. This effect can be rescued by re-expression of syndecan-3 in the lateral hypothalamus with an adeno-associated viral vector. Adeno-associated viral vector delivery of syndecan-3 to the lateral hypothalamus also reduces motivation for cocaine in normal mice. Syndecan-3 limits cocaine intake by modulating the effects of glial-cell-line-derived neurotrophic factor, which uses syndecan-3 as an alternative receptor. Our findings indicate syndecan-3-dependent signaling as a novel therapeutic target for the treatment of cocaine addiction.

Suggested Citation

  • Jihuan Chen & Vez Repunte-Canonigo & Tomoya Kawamura & Celine Lefebvre & William Shin & Leonard L. Howell & Scott E. Hemby & Brandon K. Harvey & Andrea Califano & Marisela Morales & George F. Koob & P, 2013. "Hypothalamic proteoglycan syndecan-3 is a novel cocaine addiction resilience factor," Nature Communications, Nature, vol. 4(1), pages 1-7, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2955
    DOI: 10.1038/ncomms2955
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