本文選題：阿爾茨海默病(AD) + 大鼠海馬組織�。� 參考：《中國老年學雜志》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大鼠隨機分為AD模型組和對照組,每組25只。AD模型組雙側(cè)海馬注射Aβ_(1~42),利用水迷宮實驗進行入組鼠篩選,建立AD大鼠模型,在基線記錄維持40 min后給予能誘發(fā)長時程增強(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谷氨酸受體與相關(guān)蛋白的影響。結(jié)果高頻刺激能誘導LTP持續(xù)數(shù)小時之久。實驗中通過刺激海馬區(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照組(P0.05)。結(jié)論采用水迷宮實驗能成功建立大鼠AD模型,且海馬組織可塑性變化對谷氨酸受體與相關(guān)蛋白能產(chǎn)生明顯的影響,海馬學習記憶機制參與成癮和戒斷引起的行為適應性變化。
[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，

本文編號：1987850