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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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.

First, Farber et al stated that glycine sites "may not be saturated" under physiological conditions. Recent evidence reported after Farber et al wrote their commentary supports that statement. In an extensive review of the literature, Danysza and Parsons² concluded that "NMDA receptors are clearly not saturated in vivo, because of efficient local buffering mechanisms." Similarly, Berger et al³ demonstrated significant potentiation of NMDA receptor–mediated neurotransmission by glycine and D-serine in brainstem slices, leading them to conclude that "the system is set at the most efficient point for . . . [Full Text of this Article]