Abstract
C31, consisting of 31 amino acid residues, is generated from the carboxyl terminal fragments (CTFs) of amyloid precursor protein (APP). It has been shown that C31 causes apoptosis in neurons and is present in brains of Alzheimer disease (AD) patients. Using whole-cell patch clamp techniques, we investigated effects of C31 on voltage-gated calcium channel (VGCC) currents and the protective effects of β-estradiol on PC12 cells. The results demonstrated that C31 induced a significant increase of the VGCC currents in PC12 cells, which was blocked by β-estradiol. These results suggest that modulation of intracellular calcium levels by VGCC may in part be involved in C31 induced neuronal death associated with AD.
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