Modifications induced on the amygdaloid paroxysmal activity by entopeduncolar or nigral injection of kainic acid, in the cat.

Entopeduncolar or nigral injection of kainic acid determines an early decrease of the evoked amygdaloid paroxysmal activity and a later increase of the after discharge duration. This biphasic effect is likely due to the structural analogy of the drug with monosodium glutamate, a neuroexcitant amino acid. The data suggest that the basal ganglia exert a tonic control on the amygdaloid activity.