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

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Abstract
The effect of electrolytic lesions of the ventromedial nucleus of the hypothalamus (v.m.n.) on the lordosis reflex was investigated in ovariectomized female rats. Lesions were made through chronically implanted P-I electrodes. V.m.n. lesions did not disrupt lordosis immediately, but induced a gradual decline in the reflex. Lordosis performance reached its minimum no less than 12 h after the lesion, and typically after 36-60 h. 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 co-related with lordosis deficit. Because of the slow time courses of v.m.n. lesions and stimulation (Pfaff and Sakuma, 1978) effects, the v.m.n. may not be part of the direct reflex-arc for lordosis. Neurones in v.m.n. are likely to exert a tonic hormone-dependent bias on brain stem reflex paths for this behavior.