Abstract
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 language | English (US) |
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Pages (from-to) | 180-182 |
Number of pages | 3 |
Journal | Brain research |
Volume | 716 |
Issue number | 1-2 |
DOIs | |
State | Published - Apr 15 1996 |
Externally published | Yes |
Keywords
- diazepam
- dopamine
- glutamate
- microdialysis
- prefrontal cortex
- stress
- γ-aminobutyric acid
ASJC Scopus subject areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology