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Morphological evaluation of transverse sections of retinae demonstrated a dose-dependent loss of cells in the ganglion cell layer (GCL) and a reduction in the thickness of the inner plexiform layer. No obvious alterations were noted in the more distal retinal layers. Quantitative analyses of Nissl-stained whole-mounted retinae revealed that administration of 20 nmoles of NMDA resulted in a 70% loss of cells with a soma diameter greater than 8 \u03bcm (presumed retinal ganglion cells); a 20% loss of cells with a soma diameter smaller than 8 \u03bcm (presumed displaced amacrine cells) was also observed. In addition, NMDA produced a dose-dependent decrease of retinal choline acetyltransferase (ChAT) activity, suggesting that NMDA affects cholinergic amacrine cells as well. MK-801, a non-competitive NMDA antagonist, completely prevented the NMDA-induced loss of cells in the GCL and blocked, in a dose-dependent manner, the NMDA-induced decrease of ChAT activity. The excitotoxic action of NMDA observed in these experiments is thus likely mediated through the NMDA receptor subtype. This \u201d<jats:italic>in vivo<\/jats:italic>\u201d model may be utilized to identify potential drugs that antagonize or limit the deleterious effects consequent to NMDA receptor overstimulation in the central nervous system.<\/jats:p>","DOI":"10.1017\/s0952523800005666","type":"journal-article","created":{"date-parts":[[2009,6,2]],"date-time":"2009-06-02T12:05:54Z","timestamp":1243944354000},"page":"567-573","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":217,"title":["N-methyl-D-aspartate-induced neurotoxicity in the adult rat 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