Heaton M B, Paiva M, Swanson D J, Walker D W
University of Florida Brain Institute, Department of Neuroscience, Gainesville 32610-0244.
Brain Res. 1994 Aug 22;654(2):336-42. doi: 10.1016/0006-8993(94)90497-9.
Cultures of septal and hippocampal neurons from fetal rat and dorsal root ganglion neurons from embryonic chick were pretreated with GM1 ganglioside or cycloheximide and then supplemented with toxic concentrations of ethanol. GM1 provided significant protection against ethanol neurotoxicity in each population. The inhibition of protein synthesis by cycloheximide, however, which protects against cell death resulting from withdrawal of neurotrophic factor support, did not ameliorate ethanol-induced neuronal loss.
将来自胎鼠的中隔和海马神经元以及来自胚胎鸡的背根神经节神经元培养物用GM1神经节苷脂或环己酰亚胺进行预处理,然后补充有毒浓度的乙醇。GM1对每个细胞群体中的乙醇神经毒性都提供了显著的保护作用。然而,环己酰亚胺对蛋白质合成的抑制作用虽然能防止因神经营养因子支持撤除导致的细胞死亡,但并不能改善乙醇诱导的神经元损失。