Inhibition of NFkB DNA binding activity by glucocorticoids in rat brain

Neurosci Lett. 1995 Sep 22;198(1):41-4. doi: 10.1016/0304-3940(95)11963-w.

Abstract

The influence of glucocorticoids on the transcription factor NFkB was investigated by using the gel mobility shift assay with nuclear extracts prepared from rat cerebral cortex and hippocampus after a variety of in vivo treatments. Following stimulation with each of three treatments, kainate, pilocarpine, or lithium plus pilocarpine-induced seizures, NFkB DNA binding activity was significantly greater in the cortex and hippocampus from adrenalectomized than from adrenal-intact rats. These results indicate that in rat brain glucocorticoids inhibit NFkB activity in addition to the previously reported inhibition of the transcription factor AP-1 (activator protein 1). Impairment of stimulus-induced transcription factor activity may contribute to the deleterious effects of prolonged elevations of glucocorticoids on neuronal function.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenalectomy
  • Animals
  • Base Sequence
  • Brain Chemistry / drug effects
  • Brain Chemistry / physiology*
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism
  • DNA / metabolism*
  • Excitatory Amino Acid Agonists / pharmacology
  • Glucocorticoids / physiology*
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Kainic Acid / pharmacology
  • Lithium / pharmacology
  • Male
  • Molecular Sequence Data
  • Muscarinic Agonists / pharmacology
  • NF-kappa B / biosynthesis*
  • Oxidative Stress
  • Pilocarpine / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Transcription Factor AP-1 / metabolism

Substances

  • Excitatory Amino Acid Agonists
  • Glucocorticoids
  • Muscarinic Agonists
  • NF-kappa B
  • Transcription Factor AP-1
  • Pilocarpine
  • DNA
  • Lithium
  • Kainic Acid