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新生大鼠氯胺酮麻醉后认知功能的远期改变和机制 被引量:9

The long-term changes and mechanism of cognitive function after ketamine anesthesia in neonatal rats
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摘要 目的观察新生大鼠氯胺酮麻醉后认知功能的改变及可能机制。方法新生1周Wistar大鼠30只,随机均分为3组(n=10)。对照组(CON)给予腹腔注射和氯胺酮等体积的生理盐水;K100组腹腔注射氯胺酮100mg/kg;K50组腹腔注射氯胺酮50mg/kg,每小时追加首剂量的1/2,均持续麻醉6h。麻醉后21d进行旷场实验和Morris水迷宫实验,海马标本行谷氨酸NMDAR2受体、转运体GLAST及NMDA受体亚型免疫组织化学染色,共聚焦显微镜观察并采集图像,ImageJ图像处理软件分析荧光半定量OD值。结果各组大鼠在旷场中央格的停留时间及穿越的方格数无明显差异(P〉0.05)。水迷宫测试各实验组的逃逸潜伏期均明显高于对照组(P〈0.05),探索时间短于对照组(P〈0.05),实验组之间差异不显著。麻醉处理明显增加NMDAR2、谷氨酸转运体GLAST的表达,海马CA1区NMDA受体亚型NR2A、NR2B蛋白表达增强,K100组和K50组之间并无明显不同。对照组NMDAR2受体、转运体GLAST的OD值分别为(22.0±3.0)、(20.2±2.3),K100组为(61.0±4.5)、(42.0±2.3),K50组为(58.0±4.2)、(40.0±3.3)。结论氯胺酮可降低新生大鼠认知功能,可能与上调海马NMDAR2、转运体GLAST、NR2A、NR2B表达有关。 Objective To investigate the changes and mechanism of ketamine anesthesia on cognitive function in neonatal rats. Methods 30 neonatal lweek Wistar rats were randomly divided into three groups: Group control(CON) was treated by saline with equal-volume to ketamine injection; Group K100 and Group K50 administered intraperitoneally 100mg and 50mg of ketamine for anesthetic induction respectively, and the anesthesia was maintained for 6h by administering half dose of inductive ketamine per hour. Open field and Morris water Maze were tested after 21d of anesthesia. Meanwhile, immunohistochemical techniques were implicated to observe the changes of NMDAR2, GLAST, NR2A, NR2B and NR2C at hippocampus. Results The retention time in central check and the locomotion of experimental groups were not significant different comparing with the control group( P〉 0.05). The escape latency of group K100 and group K50 was longer than control group ( P 〈 0.05 ) and the spatial probe test shorter than group CON ( P 〈 0.05), but there was no significant difference between the group K100 and group K50. Ketamine increased the expression of NMDAR2 ,GLAST, NR2A, NR2B and NR2C at hippocampus compared with control group (P〈0.05) , but there was no difference between K100 and K50 group. The OD of NMDAR and GLAST in control group, K100 group and K50 group were ( 22 ± 3.0) and (20.2 ± 2.3), (61±4.5) and (42±2.3), (58 ±4.2) and (40±2.3) respectively. Conclusion Ketamine can decrease cognitive function and this effects maybe induced by the increase of the expressions of glutamatnergic NMDAR2, GLAST, NR2A and NR2B at hippocampus in neonatal rats.
出处 《中国行为医学科学》 CSCD 2007年第9期789-791,共3页 Chinese Journal of Behavioral Medical Science
基金 陕西省社会发展科技公关项目(2003G-K10)
关键词 谷氨酸受体 谷氨酸转运体 海马 氯胺酮 免疫组织化学 Glutamatnergic receptor Glutamate transporter Hippocampus Ketamine Immunohistochemistry
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