NMDA-induced lesions of striatal cholinergic interneurons were attenua
ted by 7-chlorokynurenate (7-ClKyn), an antagonist of the glycine site
of the NMDA receptor complex. However, it was not possible to demonst
rate clearly that the mechanism of action of 7-ClKyn was in fact antag
onism of the glycine site. Thus, the agonists at the glycine site, D-s
erine and 1-aminocyclopropane-1-carboxylic acid, failed to reverse the
protection afforded by 7-ClKyn. Finally, 7-ClKyn also protected again
st lesions produced by kainate. The selectivity of 7-ClKyn under intra
cerebral administration is apparently insufficient for determining the
role of the glycine site in NMDA-receptor mediated excitotoxicity.