EXTRACELLULAR CALCIUM IS A MEDIATOR OF ASTROGLIAL INJURY DURING COMBINED GLUCOSE-OXYGEN DEPRIVATION

被引:41
作者
HAUN, SE
MURPHY, EJ
BATES, CM
HORROCKS, LA
机构
[1] OHIO STATE UNIV, DEPT PEDIAT, COLUMBUS, OH 43210 USA
[2] OHIO STATE UNIV, DEPT MED BIOCHEM, COLUMBUS, OH 43210 USA
关键词
CALCIUM; ASTROCYTE; GLIA; ISCHEMIA; HYPOXIA; CELL DEATH;
D O I
10.1016/0006-8993(92)91261-C
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We tested the hypothesis that extracellular calcium is a mediator of astroglial injury during combined glucose-oxygen deprivation. Both differentiated and undifferentiated astroglial cultures were exposed to combined glucose-oxygen deprivation in the presence and absence of extracellular calcium. Lactate dehydrogenase efflux was used as an index of cellular injury. Both types of cultures exhibited significantly less cellular injury when exposed to combined glucose-oxygen deprivation in the absence of extracellular calcium (e.g. lactate dehydrogenase efflux in undifferentiated cultures after 12 h of exposure: presence of calcium, 65.2 +/- 2.5% vs. absence of calcium, 21.4 +/- 1.3%). To further elucidate the mechanism by which extracellular calcium produces injury, we studied the effect of nimodipine, an L-type calcium channel blocker, on astroglial injury resulting from combined glucose-oxygen deprivation. Nimodipine decreased cellular injury in both types of cultures (e.g. lactate dehydrogenase efflux in undifferentiated cultures after 12 h of exposure: untreated, 65.4 +/- 2.2% vs. 10 nM nimodipine, 44.6 +/- 4.2%). Extracellular calcium appears to be a mediator of astroglial injury during combined glucose-oxygen deprivation. These results suggest that influx of extracellular calcium via L-type voltage-gated calcium channels may contribute to astroglial injury during cerebral ischemia.
引用
收藏
页码:45 / 50
页数:6
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