In experimental lead neuropathy, Schwann cells undergo segmental demyelination and possible cell death and, concurrently, remyelination and multiplication to create new internodes of myelin and onion bulb formations. In rats fed 4% lead carbonate for three months, the ability of Schwann cells to divide (percentage showing mitotic figures, labeling index, n total number per millimeter of fascicular length of nerve) was studied serially for four weeks. Schwann cell events were also compared in sural nerve distal to crush with and without resection of an intervening length of nerve. In both cases, Schwann cell multiplication as a result of axotomy was retarded in lead-intoxicated as compared to control animals. On the average, regrown myelinated axons four weeks after and 10 mm below the point of crush in lead-treated animals were similar in number and smaller in caliber, but they exhibited a normal relationship of myelin thickness to axonal area compared with control animals. These studies provide evidence that Schwann cell division and axonal regrowth after crush are retarded in experimental lead neuropathy.