The ontogenesis of peripheral sympathetic neurones was studied in the rat following subcutaneous injections of 6-hydroxydopamine (6-OH-DA), 100 mg/kg, 1, 3, and 5 days after birth. This treatment caused severe and long-lasting depletions of noradrenaline (NA) in various peripheral organs. Thirteen months after treatment, the endogenous NA content of the submaxillary gland and the spleen was 85% lower than in age-matched control animals, 70% lower in the duodenum, 60% lower in the heart, and 25% lower in the large intestine, while the catecholamine content in the adrenal glands was totally unaffected. The adrenergic cell population of the sympathetic ganglia was greatly diminished following treatment, but a few morphologically normal cells survived. These were probably responsible for the partial growth of fibers in all organs studied.Neonatal 6-OH-DA treatment also caused marked alterations in the ontogenesis of central noradrenergic neurones. The results suggest that 6-OH-DA crosses the blood–brain barrier when administered during the first week after birth, thereby causing an important impairment of terminal fiber growth in the anterior portion of the brain and spinal cord. The cell bodies localized in the brain stem are unaffected by this treatment.Although the neonatal treatment with 6-OH-DA greatly affected the ontogenesis of both peripheral and central adrenergic fibers, it did not cause a complete and permanent sympathectomy.