抄録
To investigate whether diabetes mellitus (DM) induced during early postnatal period affects myelinogenesis of the optic nerve or not, we first made neonatal-DM model rats and then carried out electron-microscopic (EM) observation and immunostaining of myelin basic protein (MBP). Neonatal-DM model rats were made by Streptozotocin injection (i.p., 100 μg/g body weight) to P2 Wistar rats. Triphasic change in the blood glucose level was found: initial sever hyperglycemia during the first 3 postnatal weeks (P4~P21), normoglycemia lasted for about two weeks (P22~P34), and mild progressive hyperglycemia after P34. Electron-microscopically, it was found in DM-rats that number of ensheathed axons was decreased in P7 and number of myelinated axons was slightly decreased in P12 and P33. Most nodes of Ranveir were abnormally formed (broad, swollen nodes) with partial axoglial dysjunction in P19. In P33, myelin lamellae were disrupted in most of myelinated axons. Immunohistochemical staining with MBP in serial sections along the entire length of the optic nerve was carried out. Migration of the oligodendrocyte precursors (OPCs) along the optic nerve from chiasmal end to eye end and sequential expression of OPCs antigens were detected in both DM group and controls. We found that number of MBP-positive cells was reduced at all levels along the entire length of the nerve in DM rats at P10. Data suggest that DM, induced during the early critical postnatal period, caused delay in the process of myelination with subsequent abnormal formation of nodal and paranodal domains. [Jpn J Physiol 54 Suppl:S217 (2004)]
