Torday C, Fónagy A, Latzkovits L
Institute of Experimental Surgery, Szent-Györgyi Albert Medical University, Szeged, Hungary.
Acta Chir Hung. 1997;36(1-4):362-3.
For better understanding of glial participation in cerebral ischemia, spectrofluorimetric analysis using the calcium indicator Fura-2AM was applied to examine the role of intracellular free Ca2+ ([Ca2+])i elevation induced by different neuroactive substances in cultured rat brain astrocytes. The activation by the general receptor agonist glutamate resulted in a biphasic cell response in [Ca2+]i. We couldn't observe N-methyl-D-aspartate-evoked [Ca2+]i response at all. Quisqualate triggered a complex [Ca2+]i response in astrocytes consisting of mobilization of Ca2+ from the intracellular stores and also Ca2+ influx from the extracellular space. Kainate elicited a markedly different Ca2+ signal an external Ca(2+)-dependent sustained [Ca2+]i rise resulting from the activation of the ionotropic glutamate receptor. According to our results two types of glutamate receptors, the quisqualate-specific metabotropic and kainate-specific ionotropic receptor, are involved in [Ca2+]i elevation in these cultures. We could monitor agonist-specific cell response to noradrenaline, serotonin, vasopressin and ATP as well in these cultured rat astrocytes.
为了更好地理解胶质细胞在脑缺血中的作用，我们应用使用钙指示剂Fura-2AM的荧光分光光度分析来研究不同神经活性物质诱导的细胞内游离Ca2+（[Ca2+]）i升高在培养的大鼠脑星形胶质细胞中的作用。一般受体激动剂谷氨酸的激活导致[Ca2+]i出现双相细胞反应。我们根本观察不到N-甲基-D-天冬氨酸诱发的[Ca2+]i反应。quisqualate在星形胶质细胞中引发了复杂的[Ca2+]i反应，包括从细胞内储存库中动员Ca2+以及细胞外空间的Ca2+内流。海人酸引发了明显不同的Ca2+信号，即由于离子型谷氨酸受体激活导致的外部Ca(2+)依赖性[Ca2+]i持续升高。根据我们的结果，两种类型的谷氨酸受体，即quisqualate特异性代谢型受体和海人酸特异性离子型受体，参与了这些培养物中[Ca2+]i的升高。我们还可以监测这些培养的大鼠星形胶质细胞中激动剂对去甲肾上腺素、5-羟色胺、血管加压素和ATP的特异性细胞反应。
