ATP, ADP, phosphocreatine (PCr), creatine (Cr), glucose, malate, sorbitol, and myo-inositol (Ml) were measured by quantitative histochemical techniques in pure neuroectodermal tissue of rat embryos of gestation days 11 and 12 that were dissected from normal and streptozocin-induced diabetic mothers. Neither gestational age nor maternal diabetes affected the tissue's energy potential (ATP-to-ADP and PCr-to-Cr ratios). Diabetes resulted in a fourfold rise in the embryonic glucose and a 25% increase in neuroectodermal malate content. Maternal hyperglycémie caused a rise in fetal sorbitol at days 11 and 12 of gestation. The Ml content of the neuroectoderm was not affected by the maternal diabetic state in prefusion embryos (day 11); however, the near doubling of Ml that occurs from day 11 to day 12 during normal development was prevented. Thus, embryos isolated from diabetic mothers on gestation day 12 had 30% less Ml than embryos isolated from normal mothers. From these data we conclude that a rise in tissue sorbitol is not always accompanied by a fall in tissue Ml. These results and recent information in the literature implicate involvement of decreased Ml concentrations in the process leading to malformation of the nervous system in diabetic embryopathy.