Greene et al and Javitt raise several points about our commentary1 on N-methyl-D-aspartate (NMDA) receptor hypofunction (NRHypo) and schizophrenia. One point concerns glycine site saturation. They correctly point out that since we wrote our commentary, new evidence was reported suggesting that the glycine site in a normal brain may not be fully saturated. However, the critical issue is the degree of glycine site saturation in schizophrenia. As we indicated in our commentary, we believe that treatment aimed at directly stimulating the glycine site would be profoundly beneficial only if the basic mechanism underlying the NRHypo state in schizophrenia were a deficiency in synaptic concentrations of glycine. Thus, evidence that direct modulation of the glycine site produces, at best, moderate improvement (eg, Tsai et al2) suggests that deficiencies in synaptic levels of glycine probably do not underlie schizophrenia.
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