CARBON-DIOXIDE INHALATION, STRESS AND ANXIOGENIC DRUGS REDUCE THE FUNCTION OF GABA(A) RECEPTOR COMPLEX IN THE RAT-BRAIN

1. The effect of different stressful stimuli on the function of the GABAA-ionophore receptor complex was evaluated by measuring the binding of 35S-TBPS to the chloride channel associated recognition sites. 2. Foot-shock stress enhanced 35S-TBPS binding in membrane preparation from rat cerebral cortex. The effect of foot-shock on 35S-TBPS binding was mimicked by the anxiogenic and proconvulsant beta-carboline FG 7142 and antagonized by anxiolytic benzodiazepines and by the novel anxiolytic and anticonvulsant beta-carboline, abecarnil. 3. A brief exposure of rats to CO2 inhalation produced, like foot-shock and FG 7142, a marked increase of 35S-TBPS binding in the cerebral cortex, cerebellum and hippocampus. The effect of CO2 inhalation was maximal 10 min after treatment and return to control value in 2 hours. Previous administration of anxiolytic drugs (alprazolam and abecarnil) completely prevented the CO2 inhalation-induced increase of 35S-TBPS binding. 4. All together these data strongly suggest that carbon dioxide inhalation, like stress and anxiogenic drugs, decreases the function of the GABAA receptor complex.