In the January 1999 issue of the ARCHIVES, Farber et al1 commented on 2 recent clinical trials of glycinergic agents used to treat schizophrenia. The commentary, overall, supported the concept that underactivity of N-methyl-D-aspartate (NMDA) receptor–mediated neurotransmission may play a crucial role in the pathophysiology of schizophrenia. However, we feel it is important to discuss 3 specific issues raised in that commentary.
Javitt DC, Heresco-Levy U. Are Glycine Sites Saturated In Vivo? Arch Gen Psychiatry. 2000;57(12):1181–1183. doi:
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