Sodium butyrate, an inhibitor of histone deacetylase, enhances drug taking and seeking behaviors in

• 作 者: JieSUN;LeiWANG;Bao-HongJIANG;BinHUI;Zhi-GangLU;LanMA;
• 机 构: Pharmacology Research Center and National Laboratory of Medical Neurobiology, Shanghai Medical Colle
• 出 处: 中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the
• 发表日期: 2007年期

　　The development of cocaine addiction involves long-lasting changes in neural plasticity and histone modification has been implicated as a potential mechanism for cocaine-induced alterations of neural plasticity.In this study,we used sodium butyrate (NaBu),a potent histone deacetylase inhibitor,able to cause hyperacetylation of core histones,to explore whether the changes in histone acetylation are relevant to cocaine-induced behavioral effects.The self-administration paradigm was used to test the effects of NaBu on cocaine taking and seeking behaviors.Our results showed that NaBu had no significant effects on sucrose-induced lever presses,but it increased cocaine-induced lever presses during cocaine self-administration and the reinstatement of drug seeking behavior induced by cocaine priming or conditioned cues (light and tone) contingent after extinction of cocaine self-administration or cocaine withdrawal.Thus,our study shows that NaBu could alter cocaine-induced behavioral plasticity and suggests that histone acetylation may play an important role in cocaine-induced behavioral plasticity.