摘要
探讨了慢性氟中毒致学习记忆损伤的脑内机制.选用初断乳雄性SD大鼠192只,随机分为4组:1个对照组,饮用自来水;3个分别饮用15,30和60 mg/L Na F溶液的染氟组.染氟期为18月.每3月用开场行为和Morris水迷宫法检测大鼠的学习记忆行为;分别在染氟中期(9月)和染氟结束后(18月)分2批断头处死大鼠,进行脑海马突触体膜流动性和海马CA3区突触后致密蛋白-95(PSD-95)表达水平等检测.结果表明:慢性氟中毒致大鼠自发活动和探究行为显著或极显著抑制,空间学习记忆能力显著下降;脑海马突触膜流动性、PSD-95表达水平均显著下降.提示慢性氟中毒致脑海马突触体膜流动性和突触后致密蛋白-95表达水平的改变可能是慢性氟中毒致学习记忆损伤的脑内突触机制之一.
The synaptic mechanism of learning-memory injury induced by chronic fluorosis in brain was inves-tigated. 192 Sprague-Dawley （SD） male rats, one-month-old, were randomly divided into four groups and given 15, 30, 60mg/L NaF solution and tap water respectively for 18 months. Behavior of rats was evaluated by open field and Morris Water Maze test every 3 months. The hippocampal synaptic membrane fluidity was detected by electron spin resonance, the expression level of post synaptic density 95 （PSD-95） in hippocam-pal CA3 region was detected by immunohistochemistry. Results showed that in rats with chronic fluorosis com-pared with the controls, locomotor activity and exploratory behavior were significantly or very significantly sup-pressed, spatial learning and memory ability were significantly declined; synaptic membrane fluidity and the protein level of PSD-95 of hippocampus were greatly decreased. The data indicated that the changes of synap-tosome membrane fluidity and PSD-95 expression level in hippocampus might be the one synaptic mechanism of learning-memory injury induced by chronic fluorosis in brain.
出处
《浙江师范大学学报（自然科学版）》
CAS
2015年第1期1-8,共8页
Journal of Zhejiang Normal University:Natural Sciences
基金
国家自然科学基金资助项目(81273015)
浙江省自然科学基金资助项目(Y2100431)
