Protein kinases and addiction

Anna M. Lee, Robert O. Messing

Research output: Chapter in Book/Report/Conference proceedingChapter

69 Scopus citations


Although drugs of abuse have different chemical structures and interact with different protein targets, all appear to usurp common neuronal systems that regulate reward and motivation. Addiction is a complex disease that is thought to involve drug-induced changes in synaptic plasticity due to alterations in cell signaling, gene transcription, and protein synthesis. Recent evidence suggests that drugs of abuse interact with and change a common network of signaling pathways that include a subset of specific protein kinases. The best studied of these kinases are reviewed here and include extracellular signal-regulated kinase, cAMP-dependent protein kinase, cyclin-dependent protein kinase 5, protein kinase C, calcium/calmodulin-dependent protein kinase II, and Fyn tyrosine kinase. These kinases have been implicated in various aspects of drug addiction including acute drug effects, drug self-administration, withdrawal, reinforcement, sensitization, and tolerance. Identifying protein kinase substrates and signaling pathways that contribute to the addicted state may provide novel approaches for new pharmacotherapies to treat drug addiction.

Original languageEnglish (US)
Title of host publicationAddiction Reviews 2008
PublisherBlackwell Publishing Inc
Number of pages36
ISBN (Print)9781573317276
StatePublished - Oct 2008
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632


  • Addiction
  • Calcium/calmodulin-dependent protein kinase II
  • Cyclin-dependent protein kinase 5
  • Extracellular signal-regulated kinase
  • Fyn tyrosine kinase
  • Protein kinase
  • Protein kinase C
  • cAMP-dependent protein kinase


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