Introduction: Alzheimer's disease (AD) is linked to neuronal calcium dyshomeostasis, which is associated with network hyperexcitability. Decreased expression of the calcium-binding protein cal-bindin-D 28K (CB) might be a susceptibility factor for AD.The subiculum is affected early in AD, for unknown reasons.
Methods:In AD, CB knock-out and control mice fluorescence Ca 2+ imaging combined with patch clamp were used to characterize Ca 2+ dynamics, resting Ca 2+ , and Ca 2+buffering capacity in subicular neurons. CB expression levels in wild-type and AD mice were also analyzed.
Results:The subiculum and dentate gyrus of wild-type mice showed age-related decline in CB expression not observed in AD mice. Resting Ca 2+ and Ca 2+ -buffering capacity was increased in aged AD mice subicular dendrites. Modeling suggests that AD calcium changes can be explained by alterations of Ca 2+ extrusion pumps rather than by buffers.
Discussion:Overall, abnormal Ca 2+ homeostasis in AD has an age dependency that comprises multiple mechanisms, including compensatory processes.
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