SummaryRepeated application of electrical stimulation to amygdala results in the progressive development and elaboration of clinical and electrographic seizures (kindling). The rate of kindling was compared in control rats and rats with various amounts of damage to the forebrain commissures. Partial or total tran‐section of corpus callosum, hippocampal commissure, and anterior commissure did not retard the rate of kindled seizure development. In the few cases in which a retarded rate of kindling was observed, there was always evidence of unintended damage to rostral thalamic nuclei; no such damage was seen in forebrain‐bisected rats that kindled at control rates. These results indicate that the forebrain commissures do not play an essential role in amygdaloid kindling, and they suggest that nuclei in the rostral thala‐mus may participate in this pheno