Lehmann A
Institute of Neurobiology, University of Göteborg, Sweden.
Neurosci Lett. 1987 Aug 31;79(3):263-6. doi: 10.1016/0304-3940(87)90440-x.
The causal role of Ca2+ in neuronal necrosis is controversial and it has been suggested that neuronal Ca2+ uptake is only a secondary effect to cell death. Here, I address this question directly by studying the morphological effects of calcium ionophore A23187 on immature cerebellar slices. Parasagittal slices were prepared and incubated for 30, 90 or 120 min in physiological saline with or without A23187. In some cases Ca2+ was omitted from the incubation medium. Slices were processed for light microscopy. A23187 produced nuclear changes indicative of cell death that encompassed cells of the external granule cell layer at short incubation times (30 min) and more deeply situated cells at longer times (120 min). This indicates that A23187 diffusion is limited in the slice. The histological changes produced by 30 min exposure to the ionophore could not be reversed by incubation for 90 min in normal medium. Necrosis was never observed when slices were exposed to A23187 in Ca2+-free medium. The results demonstrate that influx of excessive amounts of Ca2+ kills cells of the central nervous system.
钙离子在神经元坏死中的因果作用存在争议，有人认为神经元摄取钙离子只是细胞死亡的继发效应。在此，我通过研究钙离子载体A23187对未成熟小脑切片的形态学影响来直接解决这个问题。制备矢状旁切片，并在含有或不含有A23187的生理盐水中孵育30、90或120分钟。在某些情况下，孵育培养基中不含钙离子。对切片进行光学显微镜检查。A23187引起了指示细胞死亡的核变化，在短孵育时间（30分钟）时涉及外颗粒细胞层的细胞，在较长时间（120分钟）时涉及更深层的细胞。这表明A23187在切片中的扩散是有限的。暴露于离子载体30分钟所产生的组织学变化在正常培养基中孵育90分钟后无法逆转。当切片在无钙培养基中暴露于A23187时，从未观察到坏死现象。结果表明，过量钙离子的流入会杀死中枢神经系统的细胞。
