Pregnant rats were exposed to drinking water with lead (Pb) concentrations of 0, 30, or 200 mg/l. The resultant pups were sacrificed at 11, 75, and 21 d of postnatal age for the determination of synapses/mm^ in parietal cortex. Synoptic counts from electron micrographs of ethanol phosphotungstic acid stained cortical slices were counted by four observers who were blinded as to treatment (control or 200 mg Pb/l drinking water). A greater than fourfold increase in synoptic counts was observed in layers I, II, and III of rat pups parietal cortex between II and 21 d of age. Pb treatment depressed synoptic counts maximally at 15 d of age. However, Pb‐exposed pups displayed essentially the same synoptic counts us controls by 21 d of age. In a cross‐fostering design, it was shown that prenatal exposure to Pb completely accounted for the delays in synaptogeneis. No significant depression of synoptic counts was observed in pups exposed only during the postnatal period. Blood lead concentrations (Pb'B) were determined during gestation and suckling in both mother and offspring. A dramatic peripartum (partum plus and minus 4 d) peak in Pb‐B was seen in mother and pup. Pup Pb‐B peaked at 80 μg/dl at exposures of 200 mg Pb/I drinking water. In addition to being dose‐dependent, blood Pb levels resulting from the same concentration of Pb in drinking water displayed a significant dependence on litter at time‐points between birth and I yr of age. These data indicate that the substantially elevated blood Pb concentrations that are evident at partum in pups prenatally exposed to Pb might be responsible for the postnatally observed delay in synaptogenesis.