Effects of amyloid β protein fragment 25-35, AβP(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. AβP(25-35) augmented fluo-3 fluorescence of some neurons at concentrations greater than 1 μM, indicating an increase in [Ca2+]i although other neurons (about 80% of total neurons) did not respond to AβP(25-35) event at 10 μM. AβP(25-35) at 1 μM 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 AβP(25-35) increases the membrane permeability of brain neurons, resulting in a destabilized intracellular homeostasis that leads to neuonal death.
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