Histochemical staining of alkaline phosphatase was performed on liver tissue of three groups of Wistar rats: (group 1) 44 fetuses between 14 days gestational age and birth; (group 2) 76 neonatal rats between 0 and 10 days of age and; (group 3) 44 neonatal rats between 0 hr and 10 days of age, born to dams subjected to bile duct ligation 2 days before delivery.In tissue from animals ofgroup 1a progressive evolution was observed in the pattern of “canalicular‘’ staining and in the degree of positive reaction obtained.In tissue from animals ofgroup 2a striking deviation from the usual staining pattern observed at birth was seen from the 12th hr on, returning gradually to “normal‘’ by the 10th day. This change resembled different cholestatic conditions seen in tissue of adult rats. From the 6th hr until the 2nd day a slight accumulation of histochemically detectable conjugated bilirubin was observed.In animals fromgroup 3a similarly “abnormal‘’ alkaline phosphatase picture was observed at birth (0 hr), whereas no bilirubin could be visualized. The findings seen in animals ofgroup 2suggest the occurrence of a cholestatic phenomenon in early neonatal life of normal rats, presumably caused by temporary immaturity of the liver secretory function, hepatocytes or bile ducts, or both. The results found in animals ofgroup 3indicate that the sequence of changes observed in the neonatal period can be accelerated by enforcing a secretory load upon the fetal liver.SpeculationA secretory immaturity of the liver cell seen in neonatal rat liver tissue could also exist in human neonatal liver, and may be an important factor in different conditions of human neonatal jaundice. One could further speculate whether the so-called “inspissated bile syndrome” observed in young children with severe hemolysis might not be partly due to a similar immaturity of the excretory mechanisms of the liver cell