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断乳后慢性铝暴露对大鼠海马LTP及谷氨酸含量的影响

发布时间:2018-05-27 08:34

  本文选题:断乳后 +  ; 参考:《中国医科大学》2006年硕士论文


【摘要】:前言 铝(aluminum)是地壳中含量最丰富的元素之一,大量蓄积可产生神经毒性作用。国内外许多流行病学调查和研究表明,铝易致神经元损伤,引起智力和认知能力下降等学习和记忆方面的缺欠。目前动物实验已证实,铝暴露可致大鼠痴呆,其不仅表现为学习记忆的行为障碍,而且其病理形态学改变也与AD相似。 海马是学习和记忆的关键脑区,海马长时程增强(long-term potentiation,LTP)是NMDA受体依赖性突触传递效能的持续性增强,是公认的脑学习记忆功能在突触水平的研究模型和神经基础。因此研究铝暴露对LTP及与其突触机制有关的各项生化指标的影响,有助于从突触和蛋白分子水平阐明铝损害脑学习记忆功能的作用机制。目前虽然铝对LTP损害作用的观察很多,但铝对LTP损害作用的突触机制尚未完全阐明。同时,断乳后是生后脑发育的一个重要时期,海马中产生LTP的神经通路均是以谷氨酸(glutamate,Glu)为递质的。因此,本实验拟采用断乳后慢性铝暴露大鼠模型,观察中低剂量的铝暴露对海马LTP诱导和维持以及谷氨酸含量的影响,以期从递质释放角度阐明此发育阶段铝影响LTP的机制。 材料与方法 1.动物分组与染毒 生后16天的断乳Wistar大鼠60只,随机分为3组,每组20只。在饲料相同的条件下,分别自由饮用:蒸馏水(对照组)、0.2%AlCl_3水溶液(低剂量组)、0.4%AlCl_3水溶液(中剂量组)。均连续染毒80~90天,暴露期满后,改饮蒸馏水。饲养动物的室内温度18~23℃,相对湿度45~55%。
[Abstract]:Preface Aluminum is one of the most abundant elements in the crust. Many epidemiological investigations and studies at home and abroad show that aluminum is prone to neuronal damage, resulting in deficiency in learning and memory, such as decreased intelligence and cognitive ability. At present, animal experiments have proved that aluminum exposure can lead to dementia in rats, which not only shows learning and memory disorders, but also has similar pathomorphological changes to AD. Hippocampus is the key area of learning and memory. Long-term potentiation (LTP) is the continuous enhancement of NMDA receptor-dependent synaptic transmission. It is a recognized model and neural basis for the study of brain learning and memory function at synaptic level. Therefore, to study the effects of aluminum exposure on LTP and the biochemical indexes related to its synaptic mechanism is helpful to clarify the mechanism of aluminum damage to brain learning and memory function at synaptic and protein molecular level. Although there are many observations on the damage of aluminum to LTP, the synaptic mechanism of the damage of aluminum to LTP has not been fully elucidated. At the same time, postweaning is an important stage of postnatal brain development. Glutamate is the neurotransmitter in the neural pathways of LTP production in the hippocampus. Therefore, the model of chronic aluminum exposure after weaning was used to observe the effects of moderate and low doses of aluminum on LTP induction and maintenance and glutamate content in hippocampus, in order to elucidate the mechanism of aluminum affecting LTP in this developmental stage from the perspective of transmitter release. Materials and methods 1. Animal grouping and exposure Sixty weaned Wistar rats were randomly divided into 3 groups, 20 rats in each group. Under the same feed condition, the distilled water (control group, 0.2AlCl3) was drunk freely. (the low dose group was 0.4AlCl3 aqueous solution (middle dose group). All of them were poisoned continuously for 80 ~ 90 days. After the exposure expired, distilled water was changed. The indoor temperature of animals was 18 鈩,

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