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 analogu es was prevented in the mammalian nervous system by N-methyl-D-asparta te (NMDA) antagonists. The neurodegenerative effects of kainic acid, a nd the putative protection of MK-801 and 6,7-dinitroquinoxaline-2,3-di one (DNQX), were investigated by morphological studies showing the tox icity of kainic acid to the neurons of the inner nuclear layer, and me asuring choline acetyltransferase and glutamate decarboxylase activiti es in the retina. In addition, the proliferation of Muller retinal cel ls 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 exert ed a protective effect on goldfish retina]. neurons, while MK-801 did not prevent the neurotoxicity induced by kainic acid in the goldfish r etina. This finding is in agreement with previous work on kainic acid toxicity in the goldfish optic tectum.