The phenotype loss of parvalbumin-containing interneurons, characterized by decreased parvalbumin expression, has been observed in schizophrenic patients. Overproduction of intraneuronal reactive oxygen species leads to such a phenotype loss. Nuclear factor-κB (NF-κB) activation is both a target and a regulator of intracellular oxidative stress response, suggesting its involvement in the parvalbumin regulation. This study was carried out to investigate the role of the NF-κB activation in the ketamine-induced phenotype loss of parvalbumin-interneurons in vitro. Ketamine was applied to primary neuronal cultures to successfully evoke the production of increased reactive oxygen species and decreased parvalbumin expression in parvalbumin-interneurons, which was invalid in the presence of a NF-κB inhibitor, SN50 or Bay11-7082. These results suggest potential links among NF-κB activation, oxidative stress, and parvalbumin-interneurons in vitro.
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