Beta-amyloid peptide 25-35 regulates basal and hormone-stimulated Ca2+ levels in cultured rat astrocytes.

Beta-amyloid peptide (beta-AP), a characteristic constituent found in senile plaques characteristic for Alzheimer's disease, is neurotoxic by a still largely unknown mechanism. The fragment beta-AP 25-35 induces the full neurotoxic effects. It is important to understand for neurons and astrocytes the influence of beta-AP on Ca2+, a key regulator in cell toxicity and cell damage. Here we examined the effects of acute application of beta-A4 and beta-AP 25-35 on the regulation of cytosolic Ca2+ ([Ca2+]i) in rat astrocytes in primary culture. Transient [Ca2+]i rise in astrocytes induced by a brief stimulation with beta-AP was most probably due to release of Ca2+ from intracellular stores which was exacerbated by reduced extracellular Ca2+ indicating the involvement of receptors sensing extracellular Ca2+. Furthermore, P2 receptor-induced [Ca2+]i oscillations in astrocytes were reversibly interrupted by beta-AP.