6,7-Dinitroquinoxaline-2,3-dione but not MK-801 exerts a protective effect against kainic acid neurotoxicity in the goldfish retina.

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.