TRANSCRIPTIONAL OR TRANSLATIONAL INHIBITION BLOCKS LOW-DOSE NMDA-MEDIATED CELL-DEATH
TRANSCRIPTIONAL OR TRANSLATIONAL INHIBITION BLOCKS LOW-DOSE NMDA-MEDIATED CELL-DEATH
复制标题
DOI：
10.1097/00001756-199504190-00029
复制
发表时间：
1995-04-19
期刊：
影响因子：
1.7
通讯作者：
LIPTON, SA
中科院分区：
文献类型：
--
作者：
DREYER, EB;ZHANG, DX;LIPTON, SA
神经细胞中的谷氨酸毒性已得到充分证明，并可能在广泛的神经和眼科疾病中发挥作用。几个实验室最近的工作表明，在某些情况下，谷氨酸毒性可能涉及一种类似于催产素的机制。因此，我们研究了转录和翻译抑制对视网膜神经节细胞谷氨酸介导的细胞死亡的影响。我们现在报告，放线菌酮或放线菌素D可以，即使在初始兴奋性毒性损伤后2小时加入，保存视网膜神经节细胞从低剂量谷氨酸中毒。然而，放线菌酮或放线菌素D不能防止谷氨酸介导的死亡在较高浓度的兴奋毒素。这一结果表明，在低剂量下，谷氨酸的神经毒性作用可能是通过一种类似神经毒性的机制产生的。
GLUTAMATE toxicity in nerve cells has been well documented and may play a role in a broad spectrum of neurological and ophthalmic diseases. Recent work in several laboratories has suggested that an apoptotic-like mechanism may be implicated in glutamate toxicity under certain circumstances. We therefore studied the effects of transcriptional and translational inhibition on glutamate-mediated cell death in retinal ganglion cells. We now report that either cycloheximide or actinomycin D can, even when added 2 h after the initial excitotoxic insult, save retinal ganglion cells from low dose glutamate toxicity. However, cycloheximide or actinomycin D are unable to prevent glutamate-mediated death at higher concentrations of excitotoxin. This result indicates that at low doses, the neurotoxic effects of glutamate may develop through an apoptotic-like mechanism.