Dubinsky J M
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.
J Neurosci. 1993 Feb;13(2):623-31. doi: 10.1523/JNEUROSCI.13-02-00623.1993.
Intracellular calcium concentrations ([Ca2+]i) among cultured hippocampal neurons were monitored during and in the hours following an excitotoxic glutamate application to determine the time course of changes involved in delayed excitotoxicity. After a 5 min toxic insult, [Ca2+]i increased immediately and remained elevated for an hour. Subsequently, [Ca2+]i declined to normal resting levels and remained so up to 13 hr following insult. Only a few neurons displayed greatly elevated [Ca2+]i at these extended times. Survival experiments in sister cultures indicated that 85% of the neurons died after 24 hr. Therefore, intracellular calcium returned to baseline levels prior to neuronal death. Additionally, during this period when basal calcium levels had recovered, the majority of neurons responded to a second excitatory amino acid application with a second increase in [Ca2+]i.
在向培养的海马神经元施加兴奋性毒性谷氨酸期间及之后的数小时内,监测细胞内钙浓度([Ca2+]i),以确定延迟性兴奋性毒性所涉及的变化的时间进程。在5分钟的毒性损伤后,[Ca2+]i立即升高并持续1小时。随后,[Ca2+]i下降至正常静息水平,并在损伤后长达13小时保持该水平。在这些延长的时间里,只有少数神经元显示[Ca2+]i大幅升高。对姐妹培养物进行的存活实验表明,85%的神经元在24小时后死亡。因此,细胞内钙在神经元死亡之前恢复到基线水平。此外,在基础钙水平恢复的这段时间内,大多数神经元对第二次兴奋性氨基酸刺激的反应是[Ca2+]i再次升高。