Effect of amyloid β on capacitive calcium entry in neural 2a cells

We studied the direct role of amyloid β (Aβ) in regulating capacitive calcium entry (CCE), an important refilling mechanism for depleted intracellular calcium stores. For the first time, we found that Aβ can potentiate CCE. Neural 2a cells stably expressing Swedish mutant APP (APPswe), which can secrete large amounts of Aβ, have stronger CCE than its wild-type controls. Either reducing the Aβ in the medium by antibody binding or decreasing Aβ production by γ secretase inhibitor treatment could significantly depress CCE in APPswe cells. The results demonstrated that the CCE potentiation in APPswe cells was caused by Aβ over-expression. Our research also revealed that the effect of Aβ on CCE potentiation could be decreased by Aβ channel blocker, which showed that the channels formed by Aβ are one of the ways through which Aβ causes CCE potentiation.