Department of Physiology, The Royal Veterinary College, Royal College Street, London, NW1 OTU (Received 24 March 1975) Neonatal treatment of female rats with testosterone will prevent the cyclic pattern of gonadotrophin secretion and sexual receptivity in adulthood (Barraclough, 1961). This effect probably depends on the production of small amounts of oestrogen from testosterone in the brain (Reddy, Naftolin & Ryan, 1974) since non-aromatizable androgens do not have this effect (McDonald & Doughty, 1974). Antagonism of testosterone-induced masculinization by the anti-oestrogen MER-25 (ethamoxytriphetol; McDonald & Doughty, 1973/74; Doughty & McDonald, 1974) supports this hypothesis. Neonatal treatment with very low doses of the synthetic oestrogen RU 2858 (11β-methoxy-17-ethynyl-1,3,5,(10)-oestratriene-3,17β-diol) will also defeminize the female brain (Doughty, Booth, McDonald & Parrott, 1975). The object of this study was to prevent defeminization, induced by neonatal treatment with RU 2858, with the anti-oestrogen MER-25. Starting within 24 h of birth (day 1) and continuing for 5