title: GIRK Channels: A Potential Link Between Learning and Addiction.
abstract: The ability of drug-associated cues to reinitiate drug craving and seeking, even after long periods of abstinence, has led to the hypothesis that addiction represents a form of pathological learning, in which drugs of abuse hijack normal learning and memory processes to support long-term addictive behaviors. In this chapter, we review evidence suggesting that G protein-gated inwardly rectifying potassium (GIRK/Kir3) channels are one mechanism through which numerous drugs of abuse can modulate learning and memory processes. We will examine the role of GIRK channels in two forms of experience-dependent long-term changes in neuronal function: homeostatic plasticity and synaptic plasticity. We will also discuss how drug-induced changes in GIRK-mediated signaling can lead to changes that support the development and maintenance of addiction.
authors.affiliation: Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, Oregon, USA; Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota, USA. Electronic address: metipps@gmail.com.
authors.forename: Megan E
authors.initials: ME
authors.lastname: Tipps
authors.affiliation: Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, Oregon, USA; Portland Alcohol Research Center, Portland VA Medical Center, Portland, Oregon, USA.
authors.forename: Kari J
authors.initials: KJ
authors.lastname: Buck
mesh_terms: D000818:Animals; D016739:Behavior, Addictive / Q000378:metabolism*; D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels / Q000378:metabolism*; D006801:Humans; D007858:Learning / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000378:metabolism; D019966:Substance-Related Disorders / Q000378:metabolism*
chemical_list: D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels
keywords: Addiction; Depotentiation; GIRK; Homeostatic plasticity; Kir3; Learning; Memory; Synaptic plasticity