Transmission electron microscopy of synaptic ultrastructural white matter damage in neonatal rats

作     者：Baoli Yuan Sujuan Deng Zhengyu Zhang Ruilin Li 

作者机构：Department of Pediatrics Second Affiliated Hospital of Guangzhou Medical College Guangzhou 510260 Guangdong Province China Department of Histology and Embryology Guangzhou Medical College Guangzhou 510182 Guangdong Province China Department of Pediatrics Second Hospital of Xi'an Jiaotong University Xi'an 710004 Shaanxi Province China 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2010年第5卷第5期

页      面：368-371页

核心收录：

学科分类：0710[理学-生物学] 07[理学] 08[工学] 080401[工学-精密仪器及机械] 071006[理学-神经生物学] 0804[工学-仪器科学与技术] 0803[工学-光学工程] 

基　　金：the Science and Technology Program of Medical Health of Guang-zhou, No. 2008-YB-173 a Grant from Guangdong Provincial Health Depart-ment, No. A2009271 

主　　题：white matter damage myelin sheath synapse periventricular leukomalacia neural regeneration 

摘      要：BACKGROUND： To date, animal models of white matter damage remain controversial. Mild grey matter damage should be the basis for animal models to investigate white matter disease. OBJECTIVE： To establish white matter damage in neonatal rats and evaluate feasibility of the established model by observing myelination and synaptic ultrastructure. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Histology and Embryology of Guangzhou Medical College from December 2008 to May 2009. MATERIALS： H600 transmission electron microscopy was provided by Hitachi, Japan. METHODS： A total of 39 neonatal, Sprague Dawley rats were randomly assigned to normal control （n = 12）, sham-surgery （n = 12）, and white matter damage （n = 15） groups. White matter damage rats were subjected to right common carotid artery ligation, followed by inhalation of nitrogen oxygen gas mixture （6% oxygen） for 4 hours. MAIN OUTCOME MEASURES： Myelin sheath and synaptic ultrastructure in the injured （right） hippocampal CA1 region in 1-month-old rats were observed through the use of transmission electron microscopy, and pathological changes in the cerebral cortex and corpus callosum of the right hemisphere were detected by hematoxylin-eosin staining. RESULTS： Obvious tissue loss was observed in the corpus callosum of the injured （right） hemisphere. Injured oligodendrocytes and disrupted myelination were observed in the white matter damage group. However, synaptic length in the active zones, width of synaptic cleft, thickness of postsynaptic density, and curvature of the synaptic interface remained unchanged following injury, compared with the control and sham-surgery groups （P 〉 0.05）. CONCLUSION： The established white matter damage model resulted in changes in myelination and slightly altered synaptic ultrastructures. The model could function as an ideal model for white matter damage in neonatal rats.