The amygdaloid complex is functionally implicated in conditioned taste aversion (CTA) learning. Results of previous neurobehavioral studies have provided equivocal evidence concerning the involvement of specific amygdaloid nuclei in CTA learning. The present study was conducted to examine the involvement of the central (CE), lateral (LA), and basolateral (BL) amygdaloid nuclei and the temporal neocortices (area 20) in CTA learning. To that end, distinct groups of rats received bilateral electrolytic lesion placements in the CE, LA, BL, or the temporal neocortices. Control animals received scalp and meningeal incisions only. Following recovery, animals were habituated to a restricted drinking schedule with distilled water. Animals then received CTA conditioning, with LiCl used both as the conditioned stimulus and as the unconditioned stimulus. Anterograde degeneration histologies were performed on all brain tissue to evaluate relations between CTA learning deficits and axonal pathology induced by lesion placements. Results of behavioral manipulations indicated that destruction of the CE, LA, or temporal neocortex impaired CTA acquisition, but damage induced to the basolateral amygdaloid nucleus did not. Anatomical observations indicated that degeneration of amygdalofugal and/or corticofugal projections to the convolutions of the olfactory tubercle (medial), subthalamic nucleus, and the parabrachial complex is correlated with CTA learning deficits. These results indicate that destruction of the dorsolateral amygdaloid nuclei and/or the temporal neocortices may produce CTA learning deficits by affecting olfactory, gustatory, and/or gastrointestinal processing in various portions of the forebrain.