Divergent axon collaterals originate in the estrogen receptive ventromedial nucleus of hypothalamus in the rat.

The ventromedial nucleus of the hypothalamus (VMH) plays a crucial role in the mediation of lordosis by integrating predominantly inhibitory limbic signals with cyclic variation of ovarian steroids and sending a stimulatory output to the midbrain, especially the periaqueductal gray (PAG). Tract-tracing studies have established projections of the VMH 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 VMH 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 simultaneously projecting to the MPNm, MeApd, and PAG represented 7%-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 3H-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.