本文選題：斷乳后 + 鋁��； 參考：《中國(guó)醫(yī)科大學(xué)》2006年碩士論文

【摘要】：前言 鋁(aluminum)是地殼中含量最豐富的元素之一,大量蓄積可產(chǎn)生神經(jīng)毒性作用。國(guó)內(nèi)外許多流行病學(xué)調(diào)查和研究表明,鋁易致神經(jīng)元損傷,引起智力和認(rèn)知能力下降等學(xué)習(xí)和記憶方面的缺欠。目前動(dòng)物實(shí)驗(yàn)已證實(shí),鋁暴露可致大鼠癡呆,其不僅表現(xiàn)為學(xué)習(xí)記憶的行為障礙,而且其病理形態(tài)學(xué)改變也與AD相似。 海馬是學(xué)習(xí)和記憶的關(guān)鍵腦區(qū),海馬長(zhǎng)時(shí)程增強(qiáng)(long-term potentiation,LTP)是NMDA受體依賴性突觸傳遞效能的持續(xù)性增強(qiáng),是公認(rèn)的腦學(xué)習(xí)記憶功能在突觸水平的研究模型和神經(jīng)基礎(chǔ)。因此研究鋁暴露對(duì)LTP及與其突觸機(jī)制有關(guān)的各項(xiàng)生化指標(biāo)的影響,有助于從突觸和蛋白分子水平闡明鋁損害腦學(xué)習(xí)記憶功能的作用機(jī)制。目前雖然鋁對(duì)LTP損害作用的觀察很多,但鋁對(duì)LTP損害作用的突觸機(jī)制尚未完全闡明。同時(shí),斷乳后是生后腦發(fā)育的一個(gè)重要時(shí)期,海馬中產(chǎn)生LTP的神經(jīng)通路均是以谷氨酸(glutamate,Glu)為遞質(zhì)的。因此,本實(shí)驗(yàn)擬采用斷乳后慢性鋁暴露大鼠模型,觀察中低劑量的鋁暴露對(duì)海馬LTP誘導(dǎo)和維持以及谷氨酸含量的影響,以期從遞質(zhì)釋放角度闡明此發(fā)育階段鋁影響LTP的機(jī)制。 材料與方法 1.動(dòng)物分組與染毒 生后16天的斷乳Wistar大鼠60只,隨機(jī)分為3組,每組20只。在飼料相同的條件下,分別自由飲用:蒸餾水(對(duì)照組)、0.2%AlCl_3水溶液(低劑量組)、0.4%AlCl_3水溶液(中劑量組)。均連續(xù)染毒80～90天,暴露期滿后,改飲蒸餾水。飼養(yǎng)動(dòng)物的室內(nèi)溫度18～23℃,相對(duì)濕度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，

本文編號(hào)：1941277