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早老素和β-淀粉样前体蛋白对培养的大鼠海马神经元延迟整流钾通道的影响。

Effects of presenilins and beta-amyloid precursor protein on delayed rectifier potassium channels in cultured rat hippocampal neurons.

作者信息

Zhang Wei, Jin Hong-wei, Wang Xiao-liang

机构信息

Department of Pharmacology, Institute of Materia Medica, Peking Union Medical College and Chinese Academy of Medical Science, Beijing 100050, China.

出版信息

Acta Pharmacol Sin. 2004 Feb;25(2):181-5.

Abstract

AIM

To study the effects of presenilin-1 (PS-1), presenilin-2 (PS-2), and amyloid beta-protein precursor (APP695) on delayed rectifier potassium channels (IK) in the cultured rat hippocampal neurons.

METHODS

PS-1, PS-2, and APP695 were transfected into the cultured rat hippocampal neurons by transient transfection techniques. The IK current was observed by the whole cell patch-clamp techniques.

RESULTS

IK was increased in cultured rat hippocampal neurons, after transient transfection of PS-1, PS-2, and APP695. IK amplitudes and densities were significantly increased from (1689 +/- 412) pA, (48 +/- 18) pA/pF (mock cells, GFP alone, n=17) to (5565 +/- 1403) pA, (252 +/- 107) pA/pF (PS-1/GFP, n=22, P<0.01), (3804 +/- 1651) pA, (120 +/- 58) pA/pF (PS-2/GFP, n=16, P<0.01), and (4978 +/- 904) pA, (218 +/- 70) pA/pF (APP695, n=22, P<0.01). But PS-1, PS-2, and APP695 did not alter the activation curve of IK (P>0.05).

CONCLUSION

Overexpression of PS-1, PS-2, and APP695 increased IK in the cultured rat hippocampal neurons. The upregulation of IK may be related to neuronal apoptosis after PS-1, PS-2, and APP695 were transfected.

摘要

目的

研究早老素-1(PS-1)、早老素-2(PS-2)和淀粉样β蛋白前体(APP695)对培养的大鼠海马神经元延迟整流钾通道(IK)的影响。

方法

采用瞬时转染技术将PS-1、PS-2和APP695转染至培养的大鼠海马神经元。运用全细胞膜片钳技术观察IK电流。

结果

瞬时转染PS-1、PS-2和APP695后,培养的大鼠海马神经元中的IK增加。IK幅度和密度从(1689±412)pA、(48±18)pA/pF(假细胞,仅绿色荧光蛋白,n = 17)显著增加至(5565±1403)pA、(252±107)pA/pF(PS-1/绿色荧光蛋白,n = 22,P<0.01),(3804±1651)pA、(120±58)pA/pF(PS-2/绿色荧光蛋白,n = 16,P<0.01),以及(4978±904)pA、(218±70)pA/pF(APP695,n = 22,P<0.01)。但PS-1、PS-2和APP695未改变IK的激活曲线(P>0.05)。

结论

PS-1、PS-2和APP695的过表达增加了培养的大鼠海马神经元中的IK。IK的上调可能与PS-1、PS-2和APP695转染后的神经元凋亡有关。

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