Effect of a pharmacological stressor on glutamate efflux in the prefrontal cortex.
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.
Karreman
M
M
Department of Psychiatry, Yale University School of Medicine, VA Medical Center 116A/2, West Haven, CT 06516, USA.
Moghaddam
B
B
D000818:Animals; D001007:Anxiety / Q000139:chemically induced* / Q000378:metabolism*; D002243:Carbolines / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D003975:Diazepam / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D018757:GABA Modulators / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D017397:Prefrontal Cortex / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013050:Spectrometry, Fluorescence; D013315:Stress, Psychological / Q000139:chemically induced / Q000378:metabolism*
D002243:Carbolines; D018757:GABA Modulators; D018698:Glutamic Acid; C035874:FG 7142; D003975:Diazepam