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[摘要]：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-kappa B (NF-kappa B) 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-kappa B 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-kappa B inhibitor, SN50 or Bay11-7082. These results suggest potential links among NF-kappa B activation, oxidative stress, and parvalbumin-interneurons in vitro. NeuroReport 22:264-268 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins. |
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