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

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 and Pietro Paolo Sanna ()
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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
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
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

Nature Communications, 2013, vol. 4, issue 1, 1-7

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms2955

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