Abstract
In 70 rabbits, the antagonistic effects of GABA on EEG against anesthetics, chlorpromazine, sodium cyanide and asphyxia were investigated.
1. The primary effect of GABA on the EEG under phenobarbital-or urethane-anesthesia was desynchronization of high voltage slow waves. Spindle bursts were less affected by GABA. The generation of regular waves of about 5 cps. in the thalamus was another characteristic of its action. These waves were sometimes observed evidently in the cortex.
2. The high voltage slow discharge induced by relatively large dose of chlorpromazine was inhibited by GABA.
3. The high voltage slow waves generating in the cortex under cyanpoisoning were likewise desynchronized following the administration of GABA.
4. EEG-activation was observed for some minutes by an intravenous injection of a few mg. per kg. of GABA. Long lasting EEG-activation by GABA could be produced by an intravenous injection of large amount or by intravenous drip infusion.
5. GABA caused also inhibition on slow waves which generated under asphyxia.
6. Other ω-aminoacids or glutamate did not show such anti-comatose effect.
7. The EEG-activating effect of GABA became rather prominent by intracisternal injection.
8. GABA facilitated EEG-arousal by afferent stimulations under deep anesthesia.
9. The EEG-activating effect of GABA under anesthesia was observable after transection at the higher medulla, but disappeared after transection rostral to the pons.
10. Topical application of GABA on the cortex did not desynchronize slow waves.
