The effects of the putative dopaminergic antagonist, haloperidol (0.01-10 mg/kg, i.v.), on cerebral glucose utilization in 43 anatomically discrete regions of the rat brain have been examined by the quantitative autoradiographic 2-deoxyglucose technique. Dose-dependent reductions in glucose utilization were observed in 10 regions of the CNS (e.g. hippocampus, ventral thalamus and almost the entire neocortex, with the notable exception of anterior cingulate cortex). Two regions of the CNS (nucleus accumbens and pars compacta of the substantia nigra) displayed dose-related increases in glucose utilization following haloperidol administration. In addition to these specific alterations, the largest doses of haloperidol produced widespread, moderate (about 25%) reductions in glucose utilization throughout the CNS. The prior administration of haloperidol (0.1 mg/kg) prevented the effects on glucose utilization of the administration of apomorphine (1.5 mg/kg) in all regions of the CNS examined. The distribution of alterations in glucose utilization following haloperidol administration are considered in relation to the overall functional consequences of dopaminergic receptor blockade.