Effect of a pharmacological stressor on glutamate efflux in the prefrontal cortex

Mignon Karreman, Bita Moghaddam

Research output: Contribution to journalArticle

33 Scopus citations


The anxiogenic β-carboline, FG 7142 (20 mg/kg) significantly increased glutamate efflux in the prefrontal cortex of conscious rats as assessed by microdialysis. Pretreatment with the benzodiazepine receptor agonist, diazepam (5 mg/kg), abolished this effect. These findings indicate that anxiogenic compounds produce an effect similar to physical stressors on the outflow of glutamate, and implicate the GABA/benzodiazepine receptor complex in the stress-induced activation of glutamate systems in the prefrontal cortex.

Original languageEnglish (US)
Pages (from-to)180-182
Number of pages3
JournalBrain Research
Issue number1-2
Publication statusPublished - Apr 15 1996
Externally publishedYes



  • γ-aminobutyric acid
  • diazepam
  • dopamine
  • glutamate
  • microdialysis
  • prefrontal cortex
  • stress

ASJC Scopus subject areas

  • Neuroscience(all)

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