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A brief summary of the articles appearing in this issue of Biological Psychiatry.

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Review: Gamma Oscillation Models of Schizophrenia

Data from human studies have suggested that N-methyl-D-aspartate (NMDA) receptor deficits in parvalbumin-expressing (PV) inhibitory neurons may contribute to schizophrenia. This is thought to result in changes in the cortical network that manifest into positive and negative symptoms of the disease and are reflected in abnormal electroencephalography activity in schizophrenia patients. This hypothesis is being explored in several animal models of the disease, the results of which Jadi et al.

Hippocampus, Cognition, and NMDA Receptors

Anti-NMDA receptor encephalitis is an autoimmune encephalitis that manifests with a characteristic neuropsychiatric syndrome and mainly affects young women, the majority of whom suffer from persistent memory impairment despite unremarkable routine clinical magnetic resonance imaging. Investigating a large cohort of recovering patients using advanced imaging analyses, Finke et al. (pages 727–734) identify structural damage of the hippocampus that includes selective atrophy of hippocampal

Targeting NMDA Receptors to Treat Rett Syndrome

Using a circuit-based approach in wild-type and Rett syndrome mice, Mierau et al. (pages 746–754) show that NMDA receptor maturation is slower in PV interneurons than in pyramidal neurons. Loss of Mecp2, which causes Rett syndrome, accelerated the NMDA receptor subunit switch in PV cells while delaying it in pyramidal cells. Decreasing NMDA receptor GluN2A subunit expression prevented the NMDA receptor defect only in PV cells. Together, these findings indicate that PV-cell-based NMDA receptors

Ketamine: Network Effects and Stress Resilience

The brain circuits underlying the antidepressant effects of ketamine remain largely unknown. Lv et al. (pages 765–775) used resting-state functional magnetic resonance imaging to examine sustained network effects in monkeys after single-dose ketamine administration. Results show synergistic regulation of cortico-limbic-striatal circuits precisely opposing the altered brain activity observed in depressed patients. These findings suggest that local synaptic plasticity triggered by ketamine

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