Abstract
The effect of CO 2 inhalation on the function of the GABA A-coupled chloride channel was evaluated in rat brain. This treatment decreased the capability of GABA to stimulate 36Cl − uptake and produced a significant increase of [ 35S]-TBPS ([ 35S]t-butylbicyclophosphorothionate) binding in the cerebral cortex, cerebellum and hippocampus. These results demonstrate that a brief exposure of rats to CO 2 inhalation reduces the function ofthe GABA A-ionophore receptor complex in rat brain.
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