Impairments in plasticity and working memory in schizophrenia have been hypothesized to
reflect dysfunction at the N-methyl-D-aspartate glutamate receptor (NMDAR). However, the
specific mechanisms through which the NMDAR is involved in working memory versus plasticity
differ. Towards gaining a deeper understanding of how NMDAR signaling relates to individual
cognitive functions in healthy adults and patients with schizophrenia, the investigators used
a single dose of d-cycloserine (DCS) as an experimental probe to examine the effects of
enhancing NMDAR signaling on plasticity versus working memory in healthy adults and
individuals with schizophrenia.