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Rats between 5 and 45 days of age were sacrificed and their sciatic nerves dissected. Myelin was prepared from these sciatic nerves by a procedure involving purification on discontinuous sucrose gradients. The proteins of whole sciatic nerves at different ages and the proteins derived from the myelin isolated from these sciatic nerves were examined by discontinuous polyacrylamide gel electrophoresis in buffers containing sodium dodecyl sulfate. Over half of the proteins of sciatic nerve myelin migrated in a single band on the gel (P0). There were only minor changes in the protein distribution of sciatic nerve mylein during development. In contrast, the polyacrylamide gel patterns of whole sciatic nerve homogenate changed markedly during development between 5 and 15 days of age. The amount of P0 protein as a proportion of the total sciatic nerve protein increased from 3% at 5 days of age to 13% at 15 days of age after which it remained constant. Several other proteins which were also characteristic of the isolated myelin increased in relative importance during this time period. Parallel experiments dealing with a metabolic parameter of myelinogenesis, incorporation of intraperitoneally injected [35S]sulfate into sulfatide, were conducted. The maximum synthesis of sulfatide occurred between 6 and 16 days of age, coincident with the marked accumulation of myelin proteins in sciatic nerve.

Evidence of a postnatal loss of cerebral cells has been presented, based on counts of the activity of cerebral DNA following labeling with [3H]thymidine on embryonic day 14. In otherwise untreated rats, the loss was about 15 percent of the labeled cells between postnatal days 3 and 15. There was no further loss of activity thereafter. Littermates given corticosterone at day 3 showed little additional loss of labeled cells. Ganglioside NANA (N-acetylneuraminic acid) was reduced in proportion to the reduction in cerebral weight in the corticosterone treated rats. Sulfatide was reduced more, so that the concentration was 11 percent below that of the controls; It is concluded that the deficit in DNA after postnatal corticosterone treatment must be due primarily to an irreversible suppression of DNA synthesis, involving mainly glia. The reduction in gangliosides may represent a deficit in the growth of neuronal processes, leading to a reduction in the amount of neuropil, and perhaps contributing to a decrease in the number or size of myelinated axons.