The distribution of neurotensin-immunoreactive structures in the rat striatum was evaluated after blockade of dopamine neurotransmission by drugs that act presynaptically (6-hydroxydopamine, reserpine) and postsynaptically, preferentially at the D2 (eticlopride, haloperidol) and D1 [(R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepi n-7-ol, SCH-23390] receptor sites. Calbindin-D (mol. wt 28,000) immunoreactivity was used to delineate patch (striosome) and matrix in the caudate-putamen and core and shell in the nucleus accumbens. Antagonism at the D2 dopamine receptor and 6-hydroxydopamine lesions caused dense axonal immunoreactivity and moderate numbers of neurotensin-immunoreactive neurons to be distributed preferentially in the matrix of the caudate-putamen. D1 receptor antagonism was significantly less effective at eliciting neurotensin-immunoreactive neurons in the caudate-putamen. Reserpine or co-administration of the D1 and D2 receptor antagonists produced many neurotensin-immunoreactive neurons in both striatal compartments throughout the caudate-putamen and dense axonal neurotensin immunoreactivity in the medial patch compartment. To varying degrees, with SCH-23390 being least effective and reserpine most effective, all of the drug treatments elicited neurotensin immunoreactivity in neurons in the olfactory tubercle, rostral nucleus accumbens, accumbal shell and ventrolateral caudate-putamen, i.e. most of the ventral striatum.