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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Xu, Yan-Tong Robson, Matthew J. Szeszel-Fedorowicz, Wioletta Patel, Divyen Rooney, Robert McCurdy, Christopher R. Matsumoto, Rae R. |
| Description | Country affiliation: United States Author Affiliation: Xu YT ( Department of Basic Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, WV 26506, USA.) |
| Abstract | Repeated exposure to cocaine induces neuroadaptations which contribute to the rewarding properties of cocaine. Using cocaine-induced conditioned place preference (CPP) as an animal model of reward, earlier studies have shown that sigma (σ) receptor ligands can attenuate the acquisition, expression and reactivation of CPP. However, the underlying molecular mechanisms that are associated with these changes are not yet understood. In the present study, CM156, a novel antagonist with high selectivity and affinity for σ receptors was used to attenuate the expression of cocaine-induced CPP in mice. Immediately following the behavioral evaluations, mouse brain tissues were collected and alterations in gene expression in half brain samples were profiled by cDNA microarray analysis. Microarray data was analyzed by three distinct normalization methods and four genes were consistently found to be upregulated by cocaine when compared to saline controls. Each of these gene changes were found by more than one normalization method to be reversed by at least one dose of CM156. Quantitative real time PCR confirmed that a single administration of CM156 was able to reverse the cocaine-induced increases in three of these four genes: metastasis associated lung adenocarcinoma transcript 1 (malat1), tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein (ywhaz), and transthyretin (ttr). These genes are involved in processes related to neuroplasticity and RNA editing. The data presented herein provides evidence that pharmacological intervention with a putative σ receptor antagonist reverses alterations in gene expression that are associated with cocaine-induced reward. |
| File Format | HTM / HTML |
| ISSN | 00913057 |
| e-ISSN | 18735177 |
| DOI | 10.1016/j.pbb.2011.12.016 |
| Journal | Pharmacology Biochemistry and Behavior |
| Issue Number | 1 |
| Volume Number | 101 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2012-03-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Behavioral Sciences Discipline Biochemistry Discipline Pharmacology 14-3-3 Proteins Genetics Brain Chemistry Drug Effects Cocaine Antagonists & Inhibitors Conditioning, Operant Gene Expression Piperazines Pharmacology Receptors, Sigma Sulfur Compounds Analysis Of Variance Animals Behavior, Animal Binding Sites Dna, Complementary Mice Mice, Inbred C57bl Microarray Analysis Motor Activity Prealbumin Biosynthesis Isolation & Purification Rna, Long Noncoding Rna, Untranslated Real-time Polymerase Chain Reaction Reinforcement Schedule Seizures Chemically Induced Research Support, N.i.h., Extramural |
| Content Type | Text |
| Resource Type | Article |
| Subject | Biological Psychiatry Behavioral Neuroscience Biochemistry Clinical Biochemistry Toxicology Pharmacology |
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