CHANGE IN MEMBRANE-PERMEABILITY INDUCED BY AMYLOID BETA-PROTEIN FRAGMENT-25-35 IN BRAIN NEURONS DISSOCIATED FROM RATS

被引:38
作者
OYAMA, Y
CHIKAHISA, L
UEHA, T
HATAKEYAMA, Y
KOKUBUN, T
机构
[1] Laboratory of Cell Signaling (Pharmacology), Faculty of Integrated Arts and Sciences, The University of Tokushima
[2] Taiho Pharmaceutical Co., Kawauchi
[3] Meridian Instruments Far East, Inc., Tokyo 103, Chuo-ku
关键词
AMYLOID BETA-PROTEIN; BRAIN NEURON; INTRACELLULAR CA2+; MEMBRANE PERMEABILITY; VIABILITY;
D O I
10.1254/jjp.68.77
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 mu M 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.
引用
收藏
页码:77 / 83
页数:7
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