金宏伟, 张炜, 王晓良. 慢性孵育β淀粉样肽25-35对培养大鼠海马神经元电压依赖性外向钾通道亚型mRNA表达的影响J. 药学学报, 2002, 37(8): 598-602.
引用本文: 金宏伟, 张炜, 王晓良. 慢性孵育β淀粉样肽25-35对培养大鼠海马神经元电压依赖性外向钾通道亚型mRNA表达的影响J. 药学学报, 2002, 37(8): 598-602.
JIN Hong-wei, ZHANG Wei, WANG Xiao-liang. EFFECTS OF CHRONIC EXPOSURE TO BETA-AMYLOID-PEPTIDE25-35 ON THE mRNA EXPRESSIONS OF VOLTAGE-GATED OUTWARD POTASSIUM CHANNEL SUBUNITS IN CULTURED RAT HIPPOCAMPAL NEURONSJ. Acta Pharmaceutica Sinica, 2002, 37(8): 598-602.
Citation: JIN Hong-wei, ZHANG Wei, WANG Xiao-liang. EFFECTS OF CHRONIC EXPOSURE TO BETA-AMYLOID-PEPTIDE25-35 ON THE mRNA EXPRESSIONS OF VOLTAGE-GATED OUTWARD POTASSIUM CHANNEL SUBUNITS IN CULTURED RAT HIPPOCAMPAL NEURONSJ. Acta Pharmaceutica Sinica, 2002, 37(8): 598-602.

慢性孵育β淀粉样肽25-35对培养大鼠海马神经元电压依赖性外向钾通道亚型mRNA表达的影响

EFFECTS OF CHRONIC EXPOSURE TO BETA-AMYLOID-PEPTIDE25-35 ON THE mRNA EXPRESSIONS OF VOLTAGE-GATED OUTWARD POTASSIUM CHANNEL SUBUNITS IN CULTURED RAT HIPPOCAMPAL NEURONS

  • 摘要: 目的研究慢性孵育β淀粉样肽25-35(β-AP25-35)对海马神经元电压依赖性外向钾通道亚型mRNA表达的影响。方法用RT-PCR方法检测mRNA的表达,用光密度扫描法半定量测定表达变化。结果在正常培养的海马神经元上延迟整流(Kv2.1,Kv1.5),瞬间外向(A型)(Kv4.2,Kv1.4),钙激活的大电导(rSlo)钾通道亚型均有表达。β-AP25-35 3 μmol·L-1孵育细胞24 h后,Kv2.1 mRNA的表达明显上调,其它亚型则无显著性变化;β-AP25-35上调Kv2.1 mRNA的作用主要发生在β-AP25-35应用后48 h内;60 h后Kv2.1 mRNA表达水平显著下调。结论Kv2.1转录水平的上调可能参与β-AP25-35选择性地增加海马神经元上延迟整流钾电流(IK)的作用。

     

    Abstract: AIMTo investigate mRNA expression changes of voltage-gated outward potassium channel subtypes in cultured rat hippocampal neurons after chronic exposure to β-amyloid-petitde25-35 (β-AP25-35). METHODSmRNA expression was detected by RT-PCR, comparative expression levels were determined by imaging densitometer. RESULTS Delayed rectifying (Kv2.1, Kv1.5), transient outward (Kv1.4, Kv4.2) and large conductance calcium-activated (rSlo) potassium channel mRNA were expressed in cultured rat hippocampal. In the presence of β-AP25-35 3 μmol·L-1 for 24 h, the relative expression level of Kv2.1 was significantly increased (N=3, P<0.05); the other subtypes were not changed obviously (N=3, P>0.05). The increase of Kv2.1 mRNA mainly happened between 24 and 36 h after exposure to β-AP25-35. After exposure to β-AP25-35 for 60 h, Kv2.1 mRNA decreased significantly (N=3, P<0.01). CONCLUSIONThe upregulation of Kv2.1 on transcription levels may be involved in the enhancement of delayed rectifying outward potassium (IK) current induced by β-AP25-35.

     

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