Khaspekov L G, Kida E, Viktorov I V, Mossakovski M
Biull Eksp Biol Med. 1990 Sep;110(9):246-9.
A comparative morphological study of neurocytotoxic effect of quinolinic acid (QUIN) and N-methyl-D-aspartate (NMDA) in dissociated hippocampal cell culture of mouse embryos of 17-19 days' gestational age was performed. The addition of NMDA (0.2 mM) to the younger, 10 days in vitro (DIV) cultures containing immature synaptic contacts, as well as to cultures in which the mature synapses were observed (3 weeks in vitro) led to total nerve cell destruction for 24 hours. On the other hand, QUIN (0.5 mM) didn't provoke neuronal degeneration on the 10 th DIV, whereas the 21-DIV cultures exposed to QUIN showed the pronounced neurocytotoxic damage, with characteristic destruction of postsynaptic dendrites and preservation of presynaptic axon terminals. The action of toxins was blocked by specific NMDA receptor antagonist D,L-2-amino-5-phosphonovalerate. Thus, our results supplement the literature communications about the existence of NMDA-receptor subtype which mediates the neurocytotoxic effect of QUIN, and permit to suppose that these receptors appear to be expressed as far as maturation of synaptic connections occurs and functioned in the mature synaptic complex.
对孕龄17 - 19天的小鼠胚胎海马解离细胞培养物中喹啉酸(QUIN)和N - 甲基 - D - 天冬氨酸(NMDA)的神经细胞毒性作用进行了比较形态学研究。向培养10天(体外培养,DIV)、含有未成熟突触连接的较年轻培养物以及观察到成熟突触的培养物(体外培养3周)中添加NMDA(0.2 mM),24小时内导致全部神经细胞破坏。另一方面,QUIN(0.5 mM)在第10天体外培养时未引发神经元变性,而暴露于QUIN的21天体外培养物显示出明显的神经细胞毒性损伤,具有特征性的突触后树突破坏和突触前轴突终末保留。毒素的作用被特异性NMDA受体拮抗剂D,L - 2 - 氨基 - 5 - 磷酸戊酸阻断。因此,我们的结果补充了关于介导QUIN神经细胞毒性作用的NMDA受体亚型存在的文献报道,并推测这些受体似乎在突触连接成熟时表达并在成熟突触复合体中发挥作用。