Effects of different environment stimulation on nestin expression in rat hippocampus after hypoxic-ischemic brain damage
- VernacularTitle:环境刺激对缺氧缺血性脑损伤大鼠海马巢蛋白表达及学习记忆的影响
- Author:
Liqun LU
;
Congmin ZHAO
;
Zhaoxia PU
- Publication Type:Journal Article
- Keywords:
cerebral ischemia;
cerebral hypoxia;
environment;
nestin;
learning and memory
- From:Journal of Third Military Medical University
2003;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of different environment stimulation on the nestin expression in hippocampus and the ability of learning and memory of rats after hypoxic-ischemic brain damage (HIBD). Methods Rat HIBD models were established by the method of Rice in 45 SD rats, then randomly divided into three groups: standard environment stimulation group (SE), enriched environment stimulation group (EE), and impoverished environment stimulation group (IE). Another 15 rats only underwent sham-operation. Different environment intervention that was designed according to Puurunen and Bourgeon’s literatures was applied to the rats on day 2 after HIBD operation. On day 28, Morris water maze was used to evaluate the ability of learning and memory. Then the nestin expression in the hippocampus was measured by immunohistochemistry. Results The ability of learning and memory of IE group reduced and was much lower than that of sham-operation group, SE group and EE group, that of SE group was lower than that of sham-operation group and EE group, but no significant difference between sham-operation group and EE group. Immunohistochemical analysis showed that nestin expression in the hippocampus of EE group significantly increased as compared with that of other groups and that of SE group was stronger than that of sham-operation group and IE group. Conclusion The EE stimulation could increase the nestin expression in the hippocampus of neonatal rats with HIBD, enhance neuranagenesis, and improve the ability of learning and memory, while the IE stimulation could decrease the nestin expression, inhibit neuranagenesis, and impair the ability of learning and memory.
