@article{ref1,
title="Protein Kinases and Addiction",
journal="Annals of the New York Academy of Sciences",
year="2008",
author="Lee, Anna M. and Messing, Robert O.",
volume="1141",
number="1",
pages="22-57",
abstract="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.<p />",
language="en",
issn="0077-8923",
doi="10.1196/annals.1441.022",
url="http://dx.doi.org/10.1196/annals.1441.022"
}