Stix B, Reiser G
Institut für Neurobiochemie, Otto-von-Guericke-Universität Magdeburg, Medizinische Fakultät, Germany.
Neurosci Lett. 1998 Feb 27;243(1-3):121-4. doi: 10.1016/s0304-3940(98)00106-2.
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.
β-淀粉样肽（β-AP）是阿尔茨海默病特征性老年斑中的一种特征性成分，其神经毒性机制在很大程度上仍不清楚。β-AP 25-35片段可诱导完全的神经毒性作用。了解β-AP对Ca2+（细胞毒性和细胞损伤的关键调节因子）对神经元和星形胶质细胞的影响很重要。在这里，我们研究了急性应用β-A4和β-AP 25-35对原代培养大鼠星形胶质细胞胞质Ca2+（[Ca2+]i）调节的影响。β-AP短暂刺激诱导星形胶质细胞中[Ca2+]i短暂升高，很可能是由于细胞内储存的Ca2+释放，细胞外Ca2+减少会加剧这种释放，表明存在感知细胞外Ca2+的受体参与其中。此外，P2受体诱导的星形胶质细胞中[Ca2+]i振荡被β-AP可逆性中断。
