阿爾茨海默病模型大鼠海馬組織可塑性變化及其對(duì)谷氨酸受體與相關(guān)蛋白的影響
發(fā)布時(shí)間:2018-06-06 19:28
本文選題:阿爾茨海默病(AD) + 大鼠海馬組織 ; 參考:《中國(guó)老年學(xué)雜志》2017年05期
【摘要】:目的探討阿爾茨海默病(AD)大鼠海馬組織可塑性的變化及對(duì)谷氨酸受體與相關(guān)蛋白的影響。方法 50只健康雄性SD大鼠隨機(jī)分為AD模型組和對(duì)照組,每組25只。AD模型組雙側(cè)海馬注射Aβ_(1~42),利用水迷宮實(shí)驗(yàn)進(jìn)行入組鼠篩選,建立AD大鼠模型,在基線(xiàn)記錄維持40 min后給予能誘發(fā)長(zhǎng)時(shí)程增強(qiáng)(LTP)的高頻刺激,記錄f EPSP,采用經(jīng)典的蔗糖密度梯度離心來(lái)提取突觸小體、支架蛋白和Ca MKⅡα,分析AD模型大鼠海馬組織可塑性變化及對(duì)谷氨酸受體與相關(guān)蛋白的影響。結(jié)果高頻刺激能誘導(dǎo)LTP持續(xù)數(shù)小時(shí)之久。實(shí)驗(yàn)中通過(guò)刺激海馬區(qū)側(cè)支旁通路,在CA1區(qū)輻射層記錄興奮性突出后場(chǎng)電位,結(jié)果顯示:海馬區(qū)組織可塑性變化產(chǎn)生LTP并不依賴(lài)于NRB2活性;AD模型組海馬區(qū)內(nèi)谷氨酸受體及相關(guān)蛋白水平含量顯著高于對(duì)照組(P0.05)。結(jié)論采用水迷宮實(shí)驗(yàn)?zāi)艹晒⒋笫驛D模型,且海馬組織可塑性變化對(duì)谷氨酸受體與相關(guān)蛋白能產(chǎn)生明顯的影響,海馬學(xué)習(xí)記憶機(jī)制參與成癮和戒斷引起的行為適應(yīng)性變化。
[Abstract]:Objective to investigate the changes of plasticity in hippocampus of rats with Alzheimer's disease (AD) and its effects on glutamate receptors and related proteins. Methods Fifty healthy male Sprague-Dawley rats were randomly divided into AD model group (n = 25) and control group (n = 25). After maintaining the baseline record for 40 min, high frequency stimulation was given to induce long term potentiation (LTP), and f EPSPs were recorded. The synaptosomes were extracted by classical sucrose density gradient centrifugation. Scaffold protein and Ca2 + MK 鈪,
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