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Neural plasticity and addiction: PI3-kinase and cocaine behavioral sensitization

Nature Neuroscience volume 5, pages 1263–1264 (2002)Cite this article

Abstract

Drug addiction has been linked to protracted functional changes in neural circuits involved in motivation that can lead to drug dependence, craving and relapse1. Here we investigated the role of the phosphatidylinositol 3 kinase (PI3K) signal transduction pathway in long-lasting behavioral sensitization to cocaine in rats, an animal model of the long-lasting functional changes induced by repeated drug use2. Our results show that PI3K is required for the expression, but not the induction, of behavioral sensitization to cocaine.

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Figure 1: Inhibition of PI3K during the initiation phase of cocaine sensitization blocks the expression of locomotor sensitization.
Figure 2: The PI3K inhibitor LY294002 reversibly inhibits the expression of cocaine sensitization.

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Acknowledgements

This work was supported by NIH grants DA13821 and MH62140 (P.P.S.), DA08467 (F.W.) and DA04398 (G.F.K.), and a grant from the Patterson Trust (P.P.S.).

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Author notes

  1. Emanuela Izzo and Rémi Martin-Fardon: The first two authors contributed equally to this work.

Authors and Affiliations

  1. Department of Neuropharmacology, The Scripps Research Institute, 10550 N. Torrey Pines Rd., CVN12, La Jolla, 92103, California, USA

    Emanuela Izzo, Rémi Martin-Fardon, George F. Koob, Friedbert Weiss & Pietro Paolo Sanna

Authors
  1. Emanuela Izzo
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  2. Rémi Martin-Fardon
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  3. George F. Koob
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  4. Friedbert Weiss
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  5. Pietro Paolo Sanna
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Correspondence to Pietro Paolo Sanna.

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The authors declare no competing financial interests.

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Izzo, E., Martin-Fardon, R., Koob, G. et al. Neural plasticity and addiction: PI3-kinase and cocaine behavioral sensitization. Nat Neurosci 5, 1263–1264 (2002). https://doi.org/10.1038/nn977

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