中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (11): 821-826.

• 原著:退行性病与再生 • 上一篇    下一篇

Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion

  

  • 收稿日期:2011-11-01 修回日期:2012-02-24 出版日期:2012-04-15 发布日期:2012-04-15

Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion

Hui Zhao1, Zhiyong Li2, Yali Wang1, Qiuxia Zhang1   

  1. 1 School of Traditional Chinese Medicine, Capital Medical University, Beijing 100069, China
    2 China Minority Traditional Medical Center, Minzu University of China, Beijing 100081, China
  • Received:2011-11-01 Revised:2012-02-24 Online:2012-04-15 Published:2012-04-15
  • Contact: Zhiyong Li, M.D., Assistant researcher, China Minority Traditional Medical Center, Minzu University of China, Beijing 100081, China lizyong@yahoo.cn
  • About author:Hui Zhao☆, M.D., Associate professor, School of Tradi-tional Chinese Medicine, Capital Medical University, Beijing 100069, China

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Abstract:

The present study established a rat model of vascular dementia induced by chronic cerebral hypoperfusion through permanent ligation of bilateral common carotid arteries. At 60 days after modeling, escape latency and swimming path length during hidden-platform acquisition training in Morris water maze significantly increased in the model group. In addition, the number of accurate crossings over the original platform significantly decreased, hippocampal CA1 synaptophysin and growth-associated protein 43 expression significantly decreased, cAMP response element-binding protein expression remained unchanged, and phosphorylated cAMP response element-binding protein expression significantly decreased. Results suggested that abnormal expression of hippocampal synaptic structural protein and cAMP response element-binding protein phosphorylation played a role in cognitive impairment following chronic cerebral hypoperfusion.

Key words: cAMP response element-binding protein, chronic cerebral hypoperfusion, growth associated protein 43, learning and memory, synaptophysin, vascular dementia