Increases in alpha CaMKII phosphorylated on Thr286 in the nucleus   accumbens shell but not the core during priming-induced reinstatement of   morphine-seeking in rats

doi:10.1016/j.neulet.2012.07.042

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	Increases in alpha CaMKII phosphorylated on Thr286 in the nucleus accumbens shell but not the core during priming-induced reinstatement of morphine-seeking in rats
	Liu, Zhuo ; Liu, Xiao-Dong ; Zhang, Jian-Jun ; Yu, Long-Chuan
刊名	神经科学快报
	2012
关键词	Morphine self-administration Ca2+/calmodulin-dependent protein kinase II Relapse Reinstatement The nucleus accumbens DEPENDENT PROTEIN-KINASE CUE-INDUCED REINSTATEMENT COCAINE SEEKING DRUG-SEEKING GLUTAMATE RELEASE MEMORY ADDICTION DOPAMINE INVOLVEMENT RECEPTORS
DOI	10.1016/j.neulet.2012.07.042
英文摘要	Addiction is a pathological usurpation of the neural processes that normally serve reward-related learning and memory. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an important molecule involved in the mechanisms of learning and memory, suggesting its roles in drug addiction. In this study, we detected the changes of CaMKII protein levels in the nucleus accumbens (NAc), a key nucleus involved in drug-reward, during the reinstatement of morphine-seeking behavior with animal model of morphine self-administration in rats. Moreover, considering that the NAc is also involved in the natural reward-related learning and memory, we detected the changes of CaMKII protein levels in the NAc during the reinstatement of natural reward-seeking with animal model of saccharin self-administration as a control. We found that the level of alpha CaMKII phosphorylated on Thr286 increased in the NAc shell subregion but not the NAc core during the reinstatement of morphine-seeking, compared with that after extinction. However, during the reinstatement of saccharin-seeking, the protein level of alpha CaMKII phosphorylated on Thr286 did not change in the NAc shell. Surprisingly, both alpha CaMKII phosphorylated on Thr286 and beta CaMKII phosphorylated on Thr287 decreased in the NAc core during the reinstatement of saccharin-seeking. These results suggest that increased phosphorylation of CaMKII (Thr286) in the NAc shell is involved in the relapse to opioids-seeking and the mechanisms underlying the reinstatement of morphine-seeking are different from those involved in the reinstatement of natural reward-seeking. (C) 2012 Elsevier Ireland Ltd. All rights reserved.; Neurosciences; SCI(E); PubMed; 4; ARTICLE; 1; 39-44; 526
语种	英语
内容类型	期刊论文
源URL	[http://ir.pku.edu.cn/handle/20.500.11897/343198]
专题	生命科学学院
推荐引用方式 GB/T 7714	Liu, Zhuo,Liu, Xiao-Dong,Zhang, Jian-Jun,et al. Increases in alpha CaMKII phosphorylated on Thr286 in the nucleus accumbens shell but not the core during priming-induced reinstatement of morphine-seeking in rats[J]. 神经科学快报,2012.
APA	Liu, Zhuo,Liu, Xiao-Dong,Zhang, Jian-Jun,&Yu, Long-Chuan.(2012).Increases in alpha CaMKII phosphorylated on Thr286 in the nucleus accumbens shell but not the core during priming-induced reinstatement of morphine-seeking in rats.神经科学快报.
MLA	Liu, Zhuo,et al."Increases in alpha CaMKII phosphorylated on Thr286 in the nucleus accumbens shell but not the core during priming-induced reinstatement of morphine-seeking in rats".神经科学快报 (2012).