Erdö S L
Department of Anatomy, Georg-August University, Göttingen, F.R.G.
Neurosci Lett. 1990 Jul 31;115(2-3):341-4. doi: 10.1016/0304-3940(90)90479-s.
Strychnine-insensitive glycine receptors are known to modulate the toxicity of excitatory amino acids via an allosteric action at the N-methyl-D-aspartate receptor complex. To elucidate whether strychnine-sensitive glycine receptors may also influence excitotoxicity, the effect of strychnine on the excitotoxic cell death was examined in primary cultures of the rat cerebral cortex. To exclude any interference at the N-methyl-D-aspartate receptor complex, cell death was evoked by kainic acid. The release of lactic dehydrogenase (LDH) into the culture medium was taken as a quantitative measure of cell death. Strychnine reduced the excitotoxic cell death in a concentration-dependent fashion. This finding indicates that glycine may modulate the vulnerability of cortical cells to excitotoxic insults not only via the strychnine-insensitive population of glycine receptors within the N-methyl-D-aspartate receptor-complex, but also via strychnine-sensitive receptor channels.
已知对士的宁不敏感的甘氨酸受体可通过对N-甲基-D-天冬氨酸受体复合物的变构作用来调节兴奋性氨基酸的毒性。为了阐明对士的宁敏感的甘氨酸受体是否也可能影响兴奋性毒性，我们在大鼠大脑皮层原代培养物中研究了士的宁对兴奋性毒性细胞死亡的影响。为了排除对N-甲基-D-天冬氨酸受体复合物的任何干扰，我们用红藻氨酸诱发细胞死亡。将乳酸脱氢酶（LDH）释放到培养基中作为细胞死亡的定量指标。士的宁以浓度依赖的方式减少了兴奋性毒性细胞死亡。这一发现表明，甘氨酸不仅可以通过N-甲基-D-天冬氨酸受体复合物中对士的宁不敏感的甘氨酸受体群体来调节皮层细胞对兴奋性毒性损伤的易感性，还可以通过对士的宁敏感的受体通道来调节。
