The effects of gamma aminobutyric acid (GABA) upon electrocortical activity were studied with lightly anesthetized cats by applying the substance in low concentrations (0.1-1.0%) to the exposed cortical surface. Besides a suppressing action upon the sharp negative wave of 10-30 msec in duration, GABA exhibited an effect of producing high-voltage, spontaneous paroxysmal discharges.
1. The paroxysmal discharges were sustained as long as GABA remained on the cortical surface, and attained several hundred microvolts in amplitude under favorable conditions.
2. The GABA-induced paroxysmal discharges appeared as spike potentials of positive polarity, mostly occurring at a frequency of about 3 cps with or without association of slow waves. Sometimes they were composed of 0.5-3 cps slow waves having no marked spiky deflections.
3. EEG arousal, either spontaneous or produced by stimulation, and deep barbiturate anesthesia strongly suppressed the GABA-induced paroxysmal activity.
4. When KCl was applied to the GABA-treated cortical point, the preestablished paroxysmal discharge disappeared prior to the spontaneous spindle activity.
5. When the common carotid artery was occluded on both sides, the GABA-induced paroxysmal activity showed a stronger tolerance to hypoxia-anoxia produced by the circulatory arrest than the spontaneous spindle activity.
6. An electrolytic destruction of a rostral part of the thalamus of one side resulted in abolishing the pre-established paroxysmal activity at the frontal cortex ipsilateral to the thalamic lesion.
7. There could be found no marked efferent discharges of the pyramidal tract which could be related to high-voltage, paroxysmal discharges produced by GABA on the motor corte.
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