β-Amyloid peptide 25–35 regulates basal and hormone-stimulated Ca 2+ levels in cultured rat astrocytes

Abstract

β-Amyloid peptide ( β-AP), a characteristic constituent found in senile plaques characteristic for Alzheimer's disease, is neurotoxic by a still largely unknown mechanism. The fragment β-AP 25–35 induces the full neurotoxic effects. It is important to understand for neurons and astrocytes the influence of β-AP on Ca 2+, a key regulator in cell toxicity and cell damage. Here we examined the effects of acute application of β-A4 and β-AP 25–35 on the regulation of cytosolic Ca 2+ ([Ca 2+] i) in rat astrocytes in primary culture. Transient [Ca 2+] i rise in astrocytes induced by a brief stimulation with β-AP was most probably due to release of Ca 2+ from intracellular stores which was exacerbated by reduced extracellular Ca 2+ indicating the involvement of receptors sensing extracellular Ca 2+. Furthermore, P2 receptor-induced [Ca 2+] i oscillations in astrocytes were reversibly interrupted by β-AP.