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

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