Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (2): 269-272.doi: 10.3969/j.issn.1673-8225.2012.02.018

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Short-term environmental enrichment stimulation influences protein phosphorylation of Alzheimer’s disease transgenic mice

Huang Xian, Zhang Ling, Li Xue   

  1. Centre of Learning and Memory, School of Medicine, Tsinghua University, Beijing 100084, China
  • Received:2011-06-06 Revised:2011-07-16 Online:2012-01-08 Published:2012-01-08
  • Contact: Li Xue, Doctor, Engineer, Centre of Learning and Memory, School of Medicine, Tsinghua University, Beijing 100084,China lixue@mail.tsinghua.edu.cn
  • About author:Huang Xian★, Studying for master’s degree, Centre of Learning and Memory, School of Medicine, Tsinghua University, Beijing 100084, China huangxian08@gmail.com
  • Supported by:

    the Major State Basic Research Development Program of China (973 Program), No. 2011CB302201* 

Abstract:

BACKGROUND: Long-term environmental enrichment (EE) stimulation can enhance the transcription of CAMKII and CREB which are very important proteins for neuronal plasticity, learning and memory.
OBJECTIVE: To explore the effects of short-term environmental enrichment stimulation on phosphorylation of CAMKII and CREB in Alzheimer’s disease mice.
METHODS: Either C57/BL6 mice (wild type) or APP/PS1 transgenic mice were used. These laboratorial mice were assigned into three groups: APP/PS1+EE group ( long-term EE stimulations were performed when APP/PS1 transgenic mice, as Alzheimer’s disease models, were 6 months old), APP/PS1 control group (APP/PS1 transgenic mice without long-term EE stimulations) and wild-type group (wild type C57/BL6 mice). When the mice of the 3 groups reached to 18 months, each group was randomly divided into two subgroups, baseline subgroup and stimulation subgroup. The mice in every stimulation subgroup were treated with 1 day (short-term) EE stimulation.
RESULTS AND CONCLUSION: In the wild type group, the CREB phosphorylation level in the stimulation subgroup was significantly higher than that in the baseline subgroup (P < 0.05), and the CAMKII phosphorylation level had also increased. In the APP/PS1+EE group, the CAMKII phosphorylation level in the stimulation subgroup was slightly higher than that in the baseline subgroup, and there was no distinct difference in the CREB phosphorylation level between the two subgroups. In the APP/PS1 control group, there was no significant difference in CAMKII and CREB phosphorylation levels between the two subgroups. These findings suggest that short-term EE stimulation can induce an increase of CAMKII phosphorylation level in Alzheimer's disease mice only after long-term EE stimulation. However, it can obviously improve the phosphorylation level of CAMKII and CREB in wild type mice.

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