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基底外侧杏仁核Cdk5活性介导了对可卡因线索记忆的巩固与再巩固 |
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Basolateral amygdala Cdk5 activity mediates consolidation and reconsolidation of memories for cocaine cues |
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Li F-Q, Xue Y-X, Wang J-S, Fang Q, Li Y-Q, Zhu W-L, He Y-Y, Liu J-F, Xue L-F, Shaham Y, Lu L 2010/9/13 9:39:00 |
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Journal of Neuroscience, 2010, Volume 30, Issue 31
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Cocaine use and relapse involves learned associations between cocaine-associated environmental contexts and discrete stimuli and cocaine effects. Initially, these contextualanddiscrete cues undergomemoryconsolidation after being paired with cocaine exposure. During abstinence, cocaine cuememoriescan undergomemoryreconsolidation after cue exposure without the drug.Weused a conditioned place preference (CPP) procedure in rats to study the role of neuronal protein kinase cyclin-dependent kinase 5 (Cdk5) in consolidation and reconsolidation of cocaine cue memories.Wefound that the expression of cocaine CPP in drug-free tests 1 d after CPP training (four pairings of 10 mg/kg cocaine with one context and four pairings of saline with a different context) increased Cdk5 activity, and levels of the Cdk5 activator p35 in basolateral but not central amygdala. We also found that basolateral (but not central) amygdala injections of the Cdk5 inhibitor β-butyrolactone (100 ng/side) immediately (but not 6 h) after cocaine - context pairings during training prevented subsequent cocaine CPP expression. After training, acute basolateral (but not central) amygdala β-butyrolactone injections immediately before testing prevented the expression of cocaine CPP, this effect was also observed on a second test performed 1 d later, suggesting an effect on reconsolidation of cocaine cue memories. In support, basolateral β-butyrolactone injections, given immediately (but not 6 h) after a single exposure to the cocaine-paired context, prevented cocaine CPP expression 1 and 14 d after the injections. Results indicate that basolateral amygdala Cdk5 activity is critical for consolidation and reconsolidation of the memories of cocaine-associated environmental cues. Copyright © 2010 the authors.
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Correspondence Address: Wang, J.-S; School of Pharmacy, Guiyang Medical University, Guiyang 550004, China, email:jswang_yg@yahoo.com |
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疾病资源中心
王燕燕 王曙
上海交通大学附属瑞金医院内分泌科
患者,女,69岁。2009年1月无明显诱因下出现乏力,当时程度较轻,未予以重视。2009年3月患者乏力症状加重,尿色逐渐加深,大便习惯改变,颜色变淡。4月18日入我院感染科治疗,诉轻度头晕、心慌,体重减轻10kg。无肝区疼痛,无发热,无腹痛、腹泻、腹胀、里急后重,无恶性、呕吐等。入院半月前于外院就诊,查肝功能:ALT 601IU/L,AST 785IU/L,TBIL 97.7umol/L,白蛋白 41g/L,甲状腺功能:游离T3 30.6pmol/L,游离T4 51.9pmol/L,心电图示快速房颤。
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