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十溴联苯醚对大鼠学习记忆及海马神经元影响

Influence of BDE-209 exposure on learning and memory and neurons in hippocampus of adult rats

  • 摘要: 目的 探讨十溴联苯醚(BDE-209)对成年大鼠学习记忆及海马神经元的影响.方法 将48只SD成年大鼠随机分为溶剂对照组、BDE-209低、中、高(250,500,1 000 mg/kg)剂量组,每天灌胃1次,持续30 d;用Morris水迷宫测试学习记忆,电镜观察海马神经元结构.结果 对照组和BDE-209低、中、高剂量组穿越平台次数分别为(12.63±2.48)、(9.90±1.75)、(7.26±1.48)、(4.72±1.76)次,在平台象限停留时间分别为(52.92±7.78)、(31.89±5.97)、(24.82±6.65)、(18.25±5.23)s,差异具有统计学意义(P<0.05),平均逃避潜伏期随染毒剂量的增加明显延长(P<0.05);与对照组比较,BDE-209染毒组海马神经元均有不同程度损害,线粒体肿胀,粗面内质网和高尔基复合体扩张、细胞核染色质异常聚集及均匀化,神经元突触结构不清楚.结论 BDE-209可致成年大鼠海马神经元结构及其功能损伤,降低学习记忆能力.

     

    Abstract: Objective To explore the effects of brominated diphenyl ethers-209(BDE-209) exposure on spatial learning and memory abilities and ultramicrostructure of hippocampal neurons in adult rats.Methods Forty-eight Sprague Dawley adult rats were randomly divided into a solvent control group and three BDE-209-treated groups.The exposure groups were treated by intragastric administration of 250,500,and 1000 mg/kg BDE-209 once a day,respectively.The administration was lasted for 30 days.After the experiment,the capability of the learning and memory of the rats were measured with Morris water maze test.The specimens of hippocampus were sliced and morphological changes were observed under transmission electron microscopy.Results BDE-209-treated groups showed increased latencies compared with that of control group(P < 0.05).In the three BDE-209-treated groups,the latencies were increased with the increase of the dosage(P <0.05).The number of traversing the platform and the time staying in the quadrant of the original platform in four groups were 12.63±2.48,9.90±1.75,7.26±1.48,4.72±1.76 times and 52.92±7.78,31.89±5.97,24.82±6.65,18.25±5.23 seconds,with significant differences(P < 0.05 for all).The results also showed that the damages of the ultramicrostructure in hippocampal neurons were significant in the BDE-209-treated groups compared with that of the controls.Conclusion BDE-209 exposure induces structure and function damage in hippocampal neurons and the degression of learning and memory abilities of adult rats.

     

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