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Researchers have found that drugs antagonizing the N-methyl-d-aspartate receptor (NMDAR), such as phencyclidine and ketamine, produce psychotic, behavioral, and cognitive symptoms similar to schizophrenia and that NMDAR signaling has a role in information processing. These observations have prompted hypotheses about NMDAR hypofunction as a core element of the pathophysiology of schizophrenia. To study this possibility, investigators conducted a clever series of experiments using mice in which an essential NMDAR subunit (NR1) was conditionally knocked-out postnatally (a period equivalent to late gestation to age 2 years of human life), specifically in corticolimbic interneurons in which γ-aminobutyric acid (GABA) is the neurotransmitter.
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