Placement of bilateral electrolytic lesions in the mesencephalic central gray (CG) of estrogen-primed ovariectomized female rats produced an immediate decline in performance of the lordosis reflex. Lesions that destroyed the dorsal half of the CG and the adjacent subtectal region were effective. The decrease in individual animals in terms of the lordosis reflex score ranged from 20 to 100% of the prelesion performance. Such lesions abolished the facilitation of lordosis by electrical stimulation of the ventromedial nucleus of the hypothalamus. Similar abrupt losses of lordosis followed bilateral lesions of either a) the area between CG and the cuneiform nucleus of the mesencephalic reticular formation (NCf); or b) the ventrolateral quadrant of the NCf. The difference between these two lesions was that the effect of the latter could be overridden by electrical stimulation of the CG, whereas that of the former could not. We conclude that the CG is an important supraspinal component of the circuit for lordosis behavior, constituting a link between ascending somatosensory and descending motor systems for lordosis. It probably facilitates lordosis when activated by behaviorally relevant peripheral somatosensory and/or ventromedial hypothalamic inputs.