Deficit in the lordosis reflex of female rats caused by lesions in the ventromedial nucleus of the hypothalamus.

1. The effect of electrolytic lesions of the ventromedial nucleus of the hypothalamus (v.m.n.) on the lordosis reflex has been investigated on ovariectomized female rats. Lesions were made through chronically implanted platinum-iridium electrodes. 2. V.m.n. lesions did not disrupt lordosis immediately, but induced a gradual decline in the reflex. Lordosis performance reached it minimum no less than 12 hr after the lesion, and typically after 36--60 hr. 3. The magnitude of the lordosis deficit was related to the amount of v.m.n. damage. Destruction of other hypothalamic regions was without appreciable relation to the deficit. Within v.m.n., lesion size in the lateral, but not medial portion was significantly correlated with lordosis deficit. 4. Because of the slow time courses of v.m.n. lesions and stimulation (Pfaff & Sakuma, 1978) effects, it is postulated that the v.m.n. is not part of the direct reflex-arc for lordosis. Rather, neurones in v.m.n. are likely to exert a tonic hormone-dependent bias on brain stem reflex paths for this behaviour.