Previous experiments suggest that bromide ions interfere with trophic interactions of neurons in intact adult rats and may modify reactive neuroplasticity during postnatal development. Here we report on bromide effects on normal development. Rat embryos were exposed to sodium bromide (NaBr) by providing an aqueous solution of 250 mg/% NaBr in the drinking water, ad libitum, to their dams. Controls received either tap water or saline (250 mg%NaCl) to drink. Application to dams was restricted to the 5th to 15th days of gestation. Measurements of bromide concentrations in samples of blood and brain homogenates revealed, however, that bromide transfer to embryos was not restricted to the treatment period. Because of delayed excretion dams provided the offspring with bromide via placenta and milk up to 10 days after birth, although at decreasing concentrations. Significant delays in postnatal development were observed in all bromide-treated animals. Permanent deficits were recorded for body weight, brain weight and the protein content of brain tissue. Additionally, there were some changes in brain structure, e.g. the laminar structure of the neocortex was modified. In contrast to developmental deficits, the size of olfactory glomeruli was consistently larger in bromide-treated rats during postnatal and glomeruli attained a mean diameter that was 30 percent larger than in controls at 3 months of age. Results suggest that pre- and perinatal exposure of rats to moderate concentrations of NaBr may interfere with postnatal development including that of brain. Since after complete excretion of bromide developmental deficits persist and show periods of partial compensation and decompensation, induction of these bromide effects is probably indirect. The exact mechanism of bromide action on developmental processes remains to be elucidated.