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pubmed-article:7859081pubmed:abstractTextEffects of amyloid beta protein fragment 25-35, A beta P(25-35), on membrane permeability and cell viability were examined in the brain neurons dissociated from the rats using a flow cytometer and two fluorescent dyes, fluo-3 to monitor intracellular Ca2+ concentration ([Ca2+]i) of neurons and ethidium which is impermeant to membranes of intact neurons to stain dead and dying neurons. A beta P(25-35) augmented fluo-3 fluorescence of some neurons at concentrations greater than 1 microM, indicating an increase in [Ca2+]i although other neurons (about 80% of total neurons) did not respond to A beta P(25-35) even at 10 microM. A beta P(25-35) at 1 microM or greater increased dose-dependently the number of ethidium-stained neurons, suggesting a dose-dependent increase in number of dead and dying neurons. Results suggest that A beta P(25-35) increases the membrane permeability of brain neurons, resulting in a destabilized intracellular homeostasis that leads to neuonal death.lld:pubmed
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pubmed-article:7859081pubmed:articleTitleFlow cytometric analysis on cytotoxic action of amyloid beta protein fragment 25-35 on brain neurons dissociated from the rats.lld:pubmed
pubmed-article:7859081pubmed:affiliationLaboratory of Cell Signaling [Pharmacology], Faculty of Integrated Arts and Sciences, University of Tokushima, Japan.lld:pubmed
pubmed-article:7859081pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7859081pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed