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Mol. Cells 2008; 26(2): 121-130

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Gene Expression Profiling of the Rewarding Effect Caused by Methamphetamine in the Mesolimbic Dopamine System

Moon Hee Yang, Min-Suk Jung, Min Joo Lee, Kyung Hyun Yoo, Yeon Joo Yook, Eun Young Park, Seo Hee Choi, Young Ju Suh, Kee-Won Kim and Jong Hoon Park

Abstract

Methamphetamine, a commonly used addictive drug, is a powerful addictive stimulant that dramatically affects the CNS. Repeated METH administration leads to a rewarding effect in a state of addiction that includes sensitization, dependence, and other phenomena. It is well known that susceptibility to the development of addiction is influenced by sources of reinforcement, variable neuroadaptive mechanisms, and neurochemical changes that together lead to altered homeostasis of the brain reward system. These behavioral abnormalities reflect neuroadaptive changes in signal transduction function and cellular gene expression produced by repeated drug exposure. To provide a better understanding of addiction and the mechanism of the rewarding effect, it is important to identify related genes. In the present study, we performed gene expression profiling using microarray analysis in a reward effect animal model. We also investigated gene expression in four important regions of the brain, the nucleus accumbens, striatum, hippocampus, and cingulated cortex, and analyzed the data by two clustering methods. Genes related to signaling pathways including G-protein-coupled receptor-related pathways predominated among the identified genes. The genes identified in our study may contribute to the development of a gene modeling network for methamphetamine addiction.

Keywords microarray, pathway analysis, CPP, drug addiction, expression profiling, methamphetamine

Article

Research Article

Mol. Cells 2008; 26(2): 121-130

Published online August 31, 2008

Copyright © The Korean Society for Molecular and Cellular Biology.

Gene Expression Profiling of the Rewarding Effect Caused by Methamphetamine in the Mesolimbic Dopamine System

Moon Hee Yang, Min-Suk Jung, Min Joo Lee, Kyung Hyun Yoo, Yeon Joo Yook, Eun Young Park, Seo Hee Choi, Young Ju Suh, Kee-Won Kim and Jong Hoon Park

Abstract

Methamphetamine, a commonly used addictive drug, is a powerful addictive stimulant that dramatically affects the CNS. Repeated METH administration leads to a rewarding effect in a state of addiction that includes sensitization, dependence, and other phenomena. It is well known that susceptibility to the development of addiction is influenced by sources of reinforcement, variable neuroadaptive mechanisms, and neurochemical changes that together lead to altered homeostasis of the brain reward system. These behavioral abnormalities reflect neuroadaptive changes in signal transduction function and cellular gene expression produced by repeated drug exposure. To provide a better understanding of addiction and the mechanism of the rewarding effect, it is important to identify related genes. In the present study, we performed gene expression profiling using microarray analysis in a reward effect animal model. We also investigated gene expression in four important regions of the brain, the nucleus accumbens, striatum, hippocampus, and cingulated cortex, and analyzed the data by two clustering methods. Genes related to signaling pathways including G-protein-coupled receptor-related pathways predominated among the identified genes. The genes identified in our study may contribute to the development of a gene modeling network for methamphetamine addiction.

Keywords: microarray, pathway analysis, CPP, drug addiction, expression profiling, methamphetamine

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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