Cycloheximide impairs acquisition but not extinction of cocaine self-administration

被引:14
|
作者
Mierzejewski, Pawel
Siemiatkowski, Marek
Radwanska, Katarzyna
Szyndler, Janusz
Bienkowski, Przemyslaw
Stefanski, Roman
Kaczmarek, Leszek
Kostowski, Wojciech
机构
[1] Inst Psychiat & Neurol, Dept Pharmacol & Physiol Nervous Syst, PL-02957 Warsaw, Poland
[2] M Nencki Inst Expt Biol, Mol Neurobiol Lab, PL-02093 Warsaw, Poland
[3] Warsaw Med Univ, Dept Expt & Clin Pharmacol, PL-00927 Warsaw, Poland
关键词
cocaine self administration; acquisition; extinction; de novo protein synthesis; cycloheximide; drug addiction; SYNTHESIS INHIBITOR ANISOMYCIN; LONG-TERM-MEMORY; PROTEIN-SYNTHESIS; MOLECULAR-MECHANISMS; GENE-EXPRESSION; DRUG-ADDICTION; RAT; RECONSOLIDATION; NEUROSCIENCE; RETRIEVAL;
D O I
10.1016/j.neuropharm.2006.04.001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The aim of the present study was to assess the role of de novo protein synthesis in the acquisition and extinction of cocaine self-administration. In a first experiment, rats were trained to respond for intravenous cocaine infusions (0.3 mg/kg) and a protein synthesis inhibitor, cycloheximide (CHX; 3 mg/kg, s.c.) was injected immediately after each self-administration session. In a second experiment, rats were allowed to acquire cocaine self-administration and CHX was injected immediately after subsequent extinction sessions. CHX impaired the acquisition, but not extinction, of cocaine self-administration. In control experiments, CHX (3 mg/kg) blocked c-Fos protein expression after foot-shock stress and impaired the acquisition of conditioned freezing but did not inhibit spontaneous locomotor activity and sucrose drinking. Our results suggest that: i) the acquisition and extinction of cocaine-reinforced behaviour have a different molecular basis; and ii) only the former process requires de novo protein synthesis. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:367 / 373
页数:7
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