Nuclear factor-κB is involved in the phenotype loss of parvalbumin-interneurons in vitro

Neuroreport. 2011 Apr 20;22(6):264-8. doi: 10.1097/WNR.0b013e3283451787.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism*
  • Excitatory Amino Acid Antagonists / toxicity
  • Interneurons / drug effects
  • Interneurons / metabolism*
  • Ketamine / toxicity
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / agonists
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / metabolism*
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*
  • Parvalbumins / deficiency*
  • Parvalbumins / genetics
  • Phenotype*

Substances

  • Excitatory Amino Acid Antagonists
  • NF-kappa B
  • Parvalbumins
  • Ketamine