Gestational exposure to valproic acid (VPA) is a valid rodent model of human autism spectrum disorder (ASD). VPA treatment is known to bring about specific behavioral deficits of sociability, matching similar alterations in human autism. Previous quantitative morphometric studies from our laboratory showed a marked reduction and defasciculation of the mesotelencephalic DAergic pathway of VPA treated mice (injected on ED13.5, investigated on PD7), along with a decrease in tissue DA in the nucleus accumbens (NAc), but not in the caudatoputamen (CPu) (assayed by ELISA). In the present study, the correlative distribution of TH+ axons, presynaptic to the target neurons containing calretinin (CR) or calbindin (CB), was assessed using double fluorescent immunocytochemistry and confocal laser microscopy in two dopamine recipient forebrain regions, NAc and olfactory tubercle (TO) of PD7 mice. Representative image stacks were volumetrically analyzed for spatial proximity of presynaptic (TH+) and postsynaptic (CR+, CB+) structures with the help of an Imaris (Bitplane) software. In VPA mice, TH/CR juxtapositions are reduced in the NAc, and the TH/CB juxtapositions also decrease in both the NAc and (more prominently) in TO. Volume representation of CR+ and CB+ elements remained unchanged in NAc, whereas that of CB+ was markedly reduced in TO; here TH+ axons were also diminished. Interfering with the dopaminergic input to ventrobasal forebrain targets during late embryonic development will likely perturb the development and consolidation of neural and synaptic architecture, resulting in lasting changes in interneuron-type composition and synaptic density in the regions specifically involved in motivation and reward.