title: Role of ERK in cocaine addiction.
abstract: Cocaine addiction is characterized by compulsive drug-taking behavior and high rates of relapse. According to recent theories, this addiction is due to drug-induced adaptations in the cellular mechanisms that underlie normal learning and memory. Such mechanisms involve signaling by extracellular signal-regulated kinase (ERK). As we review here, evidence from rodent studies also implicates ERK in cocaine psychomotor sensitization, cocaine reward, consolidation and reconsolidation of memories for cocaine cues, and time-dependent increases in cocaine seeking after withdrawal (incubation of cocaine craving). The role of ERK in these behaviors involves long-term stable alterations in synaptic plasticity that result from repeated cocaine exposure, and also rapidly induced alterations in synaptic transmission events that acutely control cocaine-seeking behaviors. Pharmacological manipulations that decrease the extent to which cocaine and cocaine cues induce ERK activity might therefore be considered as potential treatments for cocaine addiction.
authors.affiliation: Department of Neuropharmacology, National Institute on Drug Dependence, Peking University, Beijing 100083, China. linlu@bjmu.edu.cn
authors.forename: Lin
authors.initials: L
authors.lastname: Lu
authors.forename: Eisuke
authors.initials: E
authors.lastname: Koya
authors.forename: Haifeng
authors.initials: H
authors.lastname: Zhai
authors.forename: Bruce T
authors.initials: BT
authors.lastname: Hope
authors.forename: Yavin
authors.initials: Y
authors.lastname: Shaham
mesh_terms: D000818:Animals; D001921:Brain / Q000201:enzymology*; D019970:Cocaine-Related Disorders / Q000378:metabolism / Q000503:physiopathology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000502:physiology*; D006801:Humans; D009473:Neuronal Plasticity / Q000502:physiology*
chemical_list: D048049:Extracellular Signal-Regulated MAP Kinases