Previous studies on the dopaminergic modulation of visuomotor functions in amphibians showed that the dopamine agonist apomorphine (APO) alters prey-catching strategies. After systemic administration of APO in common toads Bufo bufo, prey-oriented turning and locomotion was attenuated whereas snapping toward prey was facilitated in a dose dependent manner. With systemic APO administration, toads which had previously been hunting, that is pursuing prey, behaved in a waiting position, that is sitting motionless and waiting for prey. This suggests that APO facilitates the ingestive component and inhibits the orientational and locomotory components of prey capture. To help unravel the cerebral sites of action of APO, the present study employs the (14)C-2-deoxyglucose method to compare the rate of local glucose utilization in 41 brain structures. The retinal projection fields - e.g. superficial optic tectum, pretectal nuclei, and anterior dorsal thalamic nucleus - showed an elevation in glucose utilization due to APO-induced increases in retinal output. The medial tectal layers and the ventral striatum, both involved in visuomotor functions related to prey-oriented turning and locomotion, displayed APO-induced decreases in glucose utilization. APO-induced increases in glucose utilization were observed in the medial reticular formation and the hypoglossal nucleus which participate in the motor pattern generation of snapping. APO-induced increases in glucose utilization were also detected in the nucleus accumbens and the ventral tegmentum (mesolimbic system) as well as in the ventromedial pallium ('primordium hippocampi') and the septum, both of which belonging to the limbic system. These structures contribute to motivational level control and may be responsible for the APO-induced elevation of the snapping rate. Various other structures revealed APO-induced increases in glucose utilization. These structures include the olfactory bulb, lateral pallium, suprachiasmatic nucleus, nucleus of the periventricular organ, and the nucleus of the solitary tract. The lateral amygdala displayed APO-induced decreases in glucose utilization. The APO-induced alterations in local cerebral glucose utilization are evaluated with reference to the distribution of dopaminergic structures, and this is compared with similar data obtained in the rat by other authors. A neural network explaining the APO-induced behavioral syndrome in the common toad is discussed.