Abstract
Daily electrical stimulation of the amygdala in cats resulted in progressive development of electroclinical seizures culminating in a generalized convulsion (kindling). An electrolytic lesion in the midbrain reticular formation, ipsilateral to the stimulated amygdala, markedly elevated the generalized seizure-triggering threshold and reduced susceptibility to pentyl-entetrazol challenge. In contrast, globus palli-dus lesions had no appreciable effect upon the generalized seizure-triggering threshold and appeared to enhance susceptibility to pentylente-trazol. The results support the hypotheses that (1) the midbrain reticular formation participates significantly in the kindled amygdaloid seizures and (2) the effects of lesions in the midbrain reticular formation do not depend upon the presence of forebrain bisection.