中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2009年
6期
529-531
,共3页
银杰%南娟%杨一鸣%罗丹%蔡葵%时利德
銀傑%南娟%楊一鳴%囉丹%蔡葵%時利德
은걸%남연%양일명%라단%채규%시리덕
铝暴露%长时程增强%蛋白激酶A%断乳
鋁暴露%長時程增彊%蛋白激酶A%斷乳
려폭로%장시정증강%단백격매A%단유
Aluminum exposure%LTP%PKA%Weaning
目的 研究断乳后不同浓度慢性铝暴露对大鼠海马长时程增强及蛋白激酶A(PKA)表达的影响,进一步探讨铝损害学习与记忆的突触机制.方法 断乳的健康Wistar大鼠60只,按体质量随机平均分为3组:对照组、0.2%-Al和0.4%-Al组.各组大鼠分别自由饮用蒸馏水、Al3+ 浓度为15mmol·L-1和30mmol·L-1的A1C13水溶液;采用细胞外微电极记录法测定海马长时程增强,western-blot法测定大鼠海马内PKA蛋白表达.结果 高频刺激(HFS)后,对照组大鼠海马长时程增强发生率为77.78%,0.2%-Al组为60%、0.4%-Al组为44.44%.对照组大鼠群体锋电位平均相对幅值达基线值(144.69±29.91)%,0.2%-Al组为(113.57±16.47) %,0.4%-Al组为(103.91±19.96)%,0.4%-Al组与对照组相比,显著降低( P =0.033),但0.2%-Al组与对照组之间差异无显著性;对照组PKA含量为1.45±0.36;0.2%-Al组为1.02±0.22;0.4%-Al组为0.72±0.12.与对照组相比,2个铝暴露组大鼠海马内PKA蛋白表达显著减少( P =0.000),且2个铝暴露组间亦差异具有显著意义( P =0.000).结论 断乳后慢性铝暴露损害了海马长时程增强的表达,导致学习与记忆功能下降,可能与PKA表达的减少有关.
目的 研究斷乳後不同濃度慢性鋁暴露對大鼠海馬長時程增彊及蛋白激酶A(PKA)錶達的影響,進一步探討鋁損害學習與記憶的突觸機製.方法 斷乳的健康Wistar大鼠60隻,按體質量隨機平均分為3組:對照組、0.2%-Al和0.4%-Al組.各組大鼠分彆自由飲用蒸餾水、Al3+ 濃度為15mmol·L-1和30mmol·L-1的A1C13水溶液;採用細胞外微電極記錄法測定海馬長時程增彊,western-blot法測定大鼠海馬內PKA蛋白錶達.結果 高頻刺激(HFS)後,對照組大鼠海馬長時程增彊髮生率為77.78%,0.2%-Al組為60%、0.4%-Al組為44.44%.對照組大鼠群體鋒電位平均相對幅值達基線值(144.69±29.91)%,0.2%-Al組為(113.57±16.47) %,0.4%-Al組為(103.91±19.96)%,0.4%-Al組與對照組相比,顯著降低( P =0.033),但0.2%-Al組與對照組之間差異無顯著性;對照組PKA含量為1.45±0.36;0.2%-Al組為1.02±0.22;0.4%-Al組為0.72±0.12.與對照組相比,2箇鋁暴露組大鼠海馬內PKA蛋白錶達顯著減少( P =0.000),且2箇鋁暴露組間亦差異具有顯著意義( P =0.000).結論 斷乳後慢性鋁暴露損害瞭海馬長時程增彊的錶達,導緻學習與記憶功能下降,可能與PKA錶達的減少有關.
목적 연구단유후불동농도만성려폭로대대서해마장시정증강급단백격매A(PKA)표체적영향,진일보탐토려손해학습여기억적돌촉궤제.방법 단유적건강Wistar대서60지,안체질량수궤평균분위3조:대조조、0.2%-Al화0.4%-Al조.각조대서분별자유음용증류수、Al3+ 농도위15mmol·L-1화30mmol·L-1적A1C13수용액;채용세포외미전겁기록법측정해마장시정증강,western-blot법측정대서해마내PKA단백표체.결과 고빈자격(HFS)후,대조조대서해마장시정증강발생솔위77.78%,0.2%-Al조위60%、0.4%-Al조위44.44%.대조조대서군체봉전위평균상대폭치체기선치(144.69±29.91)%,0.2%-Al조위(113.57±16.47) %,0.4%-Al조위(103.91±19.96)%,0.4%-Al조여대조조상비,현저강저( P =0.033),단0.2%-Al조여대조조지간차이무현저성;대조조PKA함량위1.45±0.36;0.2%-Al조위1.02±0.22;0.4%-Al조위0.72±0.12.여대조조상비,2개려폭로조대서해마내PKA단백표체현저감소( P =0.000),차2개려폭로조간역차이구유현저의의( P =0.000).결론 단유후만성려폭로손해료해마장시정증강적표체,도치학습여기억공능하강,가능여PKA표체적감소유관.
Objective To study the change of LTP and the experssion of PKA in hippocampus of rats after postweaning chronic aluminum exposure of different concentration,and to go deep into the synaptic mechanism of that aluminum impairs learning and memory capacity. Methods The extracelluar microelectrode technique was used to monitor the LTP. The expression of PKA in hippocampus was measured by the method of western-blot. Results The occurrence of LTP in control group was 78.78%,in 0.2%-Al group was 60%,and in 0.4%-Al group was 44.44%.Moreover,the PS mean amplitudes relative to the baseline values after HFS in control group was(144.69±29.91)%,in 0.2%-Al group was(113.57±16.47)%,and in 0.4%-Al group was (103.91±19.96)%;compared with the control group,in 0.4%-Al group,the PS mean amplitudes relative to the baseline values were significantly decreased( P =0.033).The content of PKA in control group was 1.45±0.36,in 0.2%-Al group was 1.02±0.22,and in 0.4%-Al group was 0.72±0.12;compared to the control group,the expression of PKA in hippocampus was significantly reduced in two Al3+ exposed groups ( P =0.000),and the difference between the two exposed groups was statistically significant ( P =0.000). Conclusion Postweaning aluminum exposure can damage the expression of LTP in hippocampus of rats,consquentely impair the ability of learning and memory,which might be related to the decrease of the expression of PKA in the hippocampus.