摘要
目的 :观察产前应激 (PS)对子鼠海马神经元和神经元超微结构是否有损伤作用 ,以及这种损伤是否与氧化物的过度生成有关。方法 :采用束缚应激模型 ,观察出生后 1个月雄性子鼠的海马神经元数量、神经元超微结构及神经型一氧化氮合酶 (nNOS)表达的变化。结果 :晚期应激 (LS)引起子鼠海马CA1和CA4区的细胞数量明显减少 ;电镜可见PS使子鼠海马CA1区神经元超微结构发生改变 ,表现为线粒体肿大、边界不清、电子密度不均 ,脂褐素增多 ,偶见核变形 ;中期应激 (MS)使子鼠海马CA1、CA2、CA3区和DG内nNOS阳性表达量显著升高 ,LS使子鼠海马CA1、CA2、CA3、CA4区和DG内nNOS阳性表达量也显著升高。结论 :结果提示 ,PS对子鼠海马神经元及神经元超微结构有损伤作用 ,这种损伤可能由氧化物过度生成引起。
AIM: To investigate the effects of prenatal stress (PS) on neurons and neuronal ultrastructure of hippocampus in offspring rats, and to explore the role of the overproduction of oxidants. METHODS: One month male offspring rats were obtained to observe the neuronal number, neuronal ultrastructure and the number of nNOS -positive cell in hippocampus. RESULTS: The neuronal number of CA1 and CA4 subregions in late gestation stress (LS) offspring decreases significantly. The neuronal ultrastructure of CA1 subregion in MS (stress in 7-13 days of gestation) and LS offspring appeared bulgy mitochondria, unclear membrane and irregular electron density. Lipofuscin pigments increased; The number of nNOS-positive cell in CA1, CA2, CA3 subregions and DG of MS group and the whole hippocampus of LS group increased significantly. CONCLUSION: PS damaged the neurons and neuronal ultrastructure of hippocampus of offspring rats. The damages were associated with the overproduction of oxidants.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2003年第12期1614-1617,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .30 2 70 4 4 5 )
陕西自然科学基金重点项目 (No .2 0 0SM39)
关键词
应激
海马
氧化物
大鼠
Stress
Hippocampus
Oxides
Rats
