The effect of lead intoxication on postnatal cortical ontogenesis was studied in the 30-day-old rat. Lead encephalopathy was induced in developing Long-Evans rats by adding lead carbonate (4% w/w) to the diet of nursing mothers immediately after delivery. A segment of somatosensory neocortex was prepared for light and electron microscopy, and the neurons and the neuropil, including the synapses, were subjected to a morphometric analysis. Lead intoxication resulted in an overall reduction of gray matter which was characterized by an astrocytosis and by the preservation of the neuronal population. However, growth and maturation of the neurons in the lead rats were altered. The neurons were smaller, and, more important, the proliferation of neurite processes in the neuropil was retarded. There was also an apparent reduction in the number of synapses per neuron. However, in terms of its biochemical and morphological features, lead intoxication does not affect the maturation of the synaptic complex. The apparent effect of lead intoxication on cortical development is one of retarded neuronal maturation. This defect in neuronal maturation is proposed to be a reduction in the dendritic field and a concomitant reduction in synaptic connections.