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作 者:吕义晟[1] 祝少卿[1] 李英姿[1] 谢佐平[1]
出 处:《清华大学学报(自然科学版)》2006年第12期2040-2043,共4页Journal of Tsinghua University(Science and Technology)
基 金:北京市自然科学基金资助项目(041501117)
摘 要:为研究与淀粉样前体蛋白(am y lo id precursorprote in,APP)无关的早老素引发阿尔茨海默氏病(A lzhe im er’s d isease,AD)的致病机理,用双电极电压钳方法记录果蝇体壁肌肉细胞的钙通道。结果显示:在几种早老素突变体果蝇中,无论是正常条件下培养还是将幼虫暴露在持续稳定的高温下,电压激活的C a2+电流都没有受到影响。而撤去高温条件后,C a2+尾电流失活速度明显变慢,但其他过程不受影响。说明在正常或应激条件下并不需要早老素来维持C a2+通道的功能,但是在撤去应激条件后的一段时期内,早老素对于C a2+通道的正常功能是必要的。提示早老素对于细胞在波动环境中维持正常功能起重要作用。The linkage between presenilin incuced mutations and the pathogenesis of early onset familial Alzaeimer's disease was analyzed by studying other presenilin functions in addition to the cleavage of APP (amyloid precursor protein). The calcium and potassium currents in drosophila larva body wall muscle were recorded using the two electrode voltage clamp method. The results show that calcium currents are not affected by either normal or heat shock treatments. However, after heat shock creatments, the calcium tail currents in the mutant flies were much slower. These results indicate that presenilin is not required for maintaining Ca^2+ channel functions during either normal or stressed conditions, but is involved after the stress is removed. Presenilin is critical for maintaining Ca^2+ channels during post stress periods and, therefore, is critical for maintaining calcium homeostasis in a fluctuating environment.
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