The ventromedial nucleus of the hypothalamus ( V M H ) plays a crucial role in the mediation of lordosis by integrating predominantly inhibitory limbic signals with cyclic variation of ovarian steroids and sending a stimnlatory output to the midbrain, especially the periaqueductal gray (PAG). Tract-tracing studies have established projections of the V M H and Golgi studies have shown these neurons to frequently give rise to axon collaterals, but the anatomical pattern of shared projections has not been explored. We have used a combination of retrograde tracers to map V M H projections to the medial division of the medial preoptic nucleus ( MPNm), posterodorsal division of the medial nucleus of the amygdala (MeApd), and the PAG. Neurons with dual projections were mainly confined to the VMHvl and represented 31%-37% of each projection subset. Neurons simulta-neously prqiecting to the MPNm, MeApd, and PAG represented 70/0-9% of each projection subset. By combining tract-tracing with steroid autoradiography, we found that approximately one-quarter of each projection subset in the VMHvl concentrated 'H-estradiol. Thus, some of the VMHvl neurons that communicate a facilitatory signal to the PAG may also act to stimulate lordosis through a feedback suppression of the net inhibition formed by efferent signals from the forebrain. The even distribution of estrogen binding among projection subsets suggests a lack of compartmentalization of estrogen-regulated processes that are relevant to lordosis.