Villani L, Carraro S, Guarnieri T
Department of Biology, University of Bologna, Italy.
Neurosci Lett. 1995 Jun 9;192(2):127-31. doi: 10.1016/0304-3940(95)11616-5.
Recent findings indicated that the excitotoxicity of glutamate analogues was prevented in the mammalian nervous system by N-methyl-D-aspartate (NMDA) antagonists. The neurodegenerative effects of kainic acid, and the putative protection of MK-801 and 6,7-dinitroquinoxaline-2,3-dione (DNQX), were investigated by morphological studies showing the toxicity of kainic acid to the neurons of the inner nuclear layer, and measuring choline acetyltransferase and glutamate decarboxylase activities in the retina. In addition, the proliferation of Müller retinal cells was assumed as an index of neuronal degeneration and was quantified by counting glial fibrillary acidic protein immunopositive cells. Our observations suggest that the non-NMDA receptor antagonist DNQX exerted a protective effect on goldfish retinal neurons, while MK-801 did not prevent the neurotoxicity induced by kainic acid in the goldfish retina. This finding is in agreement with previous work on kainic acid toxicity in the goldfish optic tectum.
最近的研究结果表明，在哺乳动物神经系统中，N-甲基-D-天冬氨酸（NMDA）拮抗剂可防止谷氨酸类似物的兴奋毒性。通过形态学研究来探究红藻氨酸的神经退行性作用以及MK-801和6,7-二硝基喹喔啉-2,3-二酮（DNQX）的假定保护作用，这些研究显示了红藻氨酸对内核层神经元的毒性，并测量了视网膜中胆碱乙酰转移酶和谷氨酸脱羧酶的活性。此外，将米勒视网膜细胞的增殖作为神经元变性的指标，并通过计数胶质纤维酸性蛋白免疫阳性细胞进行量化。我们的观察结果表明，非NMDA受体拮抗剂DNQX对金鱼视网膜神经元具有保护作用，而MK-801不能预防红藻氨酸在金鱼视网膜中诱导的神经毒性。这一发现与先前关于红藻氨酸对金鱼视顶盖毒性的研究结果一致。
