The results in this article show that although electrolytic amygdala lesions disrupt learning of a conditioned taste aversion (CTA), ibotenic acid-induced, axon-sparing lesions of the amygdala do not. However, ibotenic acid lesions of the insular cortex do disrupt learning of a CTA. Electrolytic, but not ibotenic acid lesions of the amygdala, interrupt axons running between the insular (gustatory) cortex and the brain stem/hypothalamus. It is the destruction of these projections which appear to underly CTA deficits after amygdala lesions. Other results revealed that ibotenic acid lesions of the insular cortex attenuated the reaction to the novel taste of saccharin in a familiar environment but failed to affect the ingestion of a novel food in a novel environment or passive avoidance learning. Conversely, ibotenic acid lesions of the amygdala did not affect the reaction to novel saccharin in a familiar environment but did impair both the reaction to novel food in a novel environment and passive avoidance learning. We conclude that the insular cortex is involved in reactions to the novelty and associative salience exclusively of taste stimuli, whereas the amygdala is probably more concerned with the reaction to more general aspects of novelty in the environment and in fear-motivated behavior.