Ames dwarf mice do not synthesize or release growth hormone or prolactin (PRL) and have very poorly developed tuberoinfundibular dopaminergic (TIDA) neurons. An antibody to tyrosine hydroxylase (TH), the rate-limiting enzyme in the biosynthesis of dopamine, and immunohistochemical procedures were used in this study to compare the numbers of TH-immuno-positive neurons observed in the arcuate nuclei of Ames dwarf mice compared to phenotypically normal mice of the same strain. In female dwarfs, the number of TH-immunopositive neurons in the arcuate nuclei but not the pars compacta was markedly reduced when compared to normal females. The elevation of circulating PRL either by the implantation of a normal pituitary under the kidney capsule or by the daily administration of ovine PRL increased the numbers of arcuate neurons which expressed immunochemically detectable TH to a level comparable to that observed in untreated normal mice. The number of TH-expressing neurons was also reduced in the arcuate nuclei of dwarf males although the deficiency was not as great as in females. Ovine PRL seemed to have little effect on the numbers of TH-immunopositive neurons observed in either dwarf or normal male mice. These results suggest that the postnatal absence of PRL in mice does not result in a major reduction in the total population of TIDA neurons. Rather these neurons appear to be present in nearly normal numbers but are in a dormant state in the absence of circulating PRL.