Oyama Y, Chikahisa L, Ueha T, Hatakeyama Y, Kokubun T
Laboratory of Cell Signaling (Pharmacology), Faculty of Integrated Arts and Sciences, University of Tokushima, Japan.
Jpn J Pharmacol. 1995 May;68(1):77-83. doi: 10.1254/jjp.68.77.
Effects of amyloid beta-protein fragment 25-35, A beta P(25-35), on the membrane permeability of organic molecules were examined in the brain neurons dissociated from rats by using an argon laser (equipped in flow cytometer and laser microscope) and a combination of two fluorescent dyes, fluo-3-AM and ethidium bromide. A beta P(25-35) at concentrations of 1 microM or greater induced both leakage of fluo-3 from the neurons and permeation of ethidium across the membrane in a dose-dependent manner, although both dyes are highly impermeant to the intact plasma membrane. Thus, A beta P(25-35) seems to increase not only membrane permeability of inorganic ions such as Ca2+, Na+ and K+, as previously suggested, but also that of organic molecules. Therefore, the brain neuron membrane is suggested to lose its integrity in the presence of A beta P(25-35) that leads to neuronal death.
采用氩激光（配备于流式细胞仪和激光显微镜中）以及两种荧光染料（fluo-3-AM和溴化乙锭）的组合，研究了β淀粉样蛋白片段25 - 35（AβP(25 - 35)）对大鼠离体脑神经元中有机分子膜通透性的影响。尽管这两种染料对于完整的质膜具有高度的不可渗透性，但浓度为1微摩尔或更高的AβP(25 - 35)会以剂量依赖的方式诱导fluo-3从神经元中泄漏以及溴化乙锭透过膜。因此，AβP(25 - 35)似乎不仅如先前所表明的那样增加无机离子如Ca2 +、Na +和K +的膜通透性，还增加有机分子的膜通透性。所以，在导致神经元死亡的AβP(25 - 35)存在的情况下，脑神经元膜被认为会丧失其完整性。
