Karreman M, Moghaddam B
Department of Psychiatry, Yale University School of Medicine, VA Medical Center 116A/2, West Haven, CT 06516, USA.
Brain Res. 1996 Apr 15;716(1-2):180-2. doi: 10.1016/0006-8993(96)00015-7.
The anxiogenic beta-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.
