Abstract
Relationship between learning-memory function impairment and synaptophysin expression in hippocampus of rats with ischemia reperfusion injury
  
DOI:
EN KeyWords: Ischemia-reperfusion  Learning-memory  Hippocampus  Synaptophysin
Fund Project:国家自然科学基金资助项目(81403462);福建省教育厅资助省属高校项目(JK2014022)
作者单位
李建鸿 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
黄佳 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
宋长明 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
杨敏光 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
金婷婷 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
柳维林 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
陶静 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
陈立典 福建中医药大学康复医学院福建省康复技术重点实验室福建康复产业研究院技术创新平台国家中医药管理局中医康复研究中心福州 350122 
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EN Abstract:
  Objective:To observe the impairment of learning and memory ability and its correlation with synaptophysin (SYN) protein expression in hippocampus of rats with ischemia-reperfusion injury. Methods: Sixteen male Sprague-Dawley (SD) rats raised in SPF were randomly divided into model (n=10) and control (n=6) groups. Rats in the model group were treated with the modified Longa' methods to create the left middle cerebral artery occlusion (MCAO) model. Rats of the model (n=6) and the control (n=6) groups that met the inclusion criteria were included. Neurological deficit was assessed by Zea Longa neurobehavioral scores tests. T2 weighted image (T2WI) scan was used to observe the volume of cerebral infarction in rats. The function of learning and memory was tested by Barnes maze. The SYN expression in the hippocampus was detected by Western blotting. The correlation between the expression level of SYN in the model group and the escape latency of rats and the number of entrance into the wrong holes was analyzed. Results: After 2 h of operation, the Zea-Longa scores in the model group increased and the symptoms of neurological deficits appeared; After 24 h of operation, T2WI scan showed that the model group had cerebral infarction. As compared with the control group, the Barnes data showed that the escape latency in the model group was significantly prolonged (P<0.01), and the number of times into the wrong holes was significantly increased (P<0.01); the expression of SYN in the hippocampus of the model group was significantly decreased (P<0.01). Correlation analysis showed that the expression level of SYN was significantly negatively correlated with the escape latency for a correct hole and the number of times into the wrong holes. The correlation coefficient between SYN expression level and the escape latency of rats was r=-0.916 (P<0.05); the correlation coefficient between SYN expression level and the number of rats entering the wrong entrance holes was r=-0.87 (P<0.05). Conclusion: The impairment of learning and memory function in rats with cerebral ischemia-reperfusion injury may be related to the decrease of SYN expression in the hippocampus, which may result in the damage of synaptic plasticity.
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