Erdö S L, Cai N, Lakics V
CNS Pharmacology Laboratory, Chinoin Co. Ltd., Budapest, Hungary.
Neurosci Lett. 1993 Apr 2;152(1-2):84-6. doi: 10.1016/0304-3940(93)90489-8.
The excitotoxic cell death and the release of gamma-amino-butyric acid (GABA) evoked by excitatory amino acids (EAAs) were comparatively examined in rat cortical sister cultures grown in serum-free (N2) and serum-supplemented (SSM) media. Cell death was induced by 24 h exposure to 1 mM N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) or kainate. [3H]GABA release was evoked by 5 min exposure of preloaded cultures to 0.5 mM NMDA, AMPA or kainate. EAAs evoked remarkable GABA release in both N2 and SSM cultures, but caused toxic cell death in SSM cultures, only. Our findings indicate that functionally active EAA receptors do not necessarily mediate neurotoxicity and suggest that excitotoxicity can be prevented without blocking excitatory transmission.
在无血清（N2）和补充血清（SSM）培养基中生长的大鼠皮质姐妹培养物中，对兴奋性氨基酸（EAA）诱发的兴奋性毒性细胞死亡和γ-氨基丁酸（GABA）释放进行了比较研究。通过将细胞暴露于1 mM N-甲基-D-天冬氨酸（NMDA）、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）或红藻氨酸24小时来诱导细胞死亡。通过将预加载的培养物暴露于0.5 mM NMDA、AMPA或红藻氨酸5分钟来诱发[3H]GABA释放。EAA在N2和SSM培养物中均诱发了显著的GABA释放，但仅在SSM培养物中导致毒性细胞死亡。我们的研究结果表明，功能活跃的EAA受体不一定介导神经毒性，并表明在不阻断兴奋性传递的情况下可以预防兴奋性毒性。
