NMDA-induced lesions of striatal cholinergic interneurons were attenuated by 7-chlorokynurenate (7-ClKyn), an antagonist of the glycine site of the NMDA receptor complex. However, it was not possible to demonstrate clearly that the mechanism of action of 7-ClKyn was in fact antagonism of the glycine site. Thus, the agonists at the glycine site, d-serine and 1-aminocyclopropane-1-carboxylic acid, failed to reverse the protection afforded by 7-ClKyn. Finally, 7-ClKyn also protected against lesions produced by kainate. The selectivity of 7-ClKyn under intracerebral administration is apparently insufficient for determining the role of the glycine site in NMDA-receptor mediated excitotoxicity. © 1993.
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