Uteroplacental insufficiency often results in asymmetric IUGR. Despite sparing of brain growth, IUGR infants are at significant risk for ischemic neurological damage as well as neurodevelopmental delay. Mitochondrial electron transport is a primary source of free radical production which leads to subsequent lipid peroxidation associated with ischemia. As a result, we hypothesized that cerebral gene expression of key mitochondrial proteins NADH dehydrogenase subunit 4 (ND4) (a complex I subunit), subunit C(SC) of the mitochondrial ATPase, and the adenine nucleotide translocases (A1 and A2) would be altered in IUGR fetal and juvenile rats. We performed bilateral uterine artery ligation to induce asymmetric IUGR and sham surgery (C) in pregnant rats on day 19 of gestation. Cerebral tissue was harvested on day 20(F20), 21 (F21) of fetal life, and day 4 (J4), 14 (J14), 21 (J21) of neonatal life. To measure mRNA levels, we used RTPCR with an internal control. Gene expression of all four enzymes were significantly increased in IUGR F20 brain(C=1.0, ND4=2.45, SC=1.75, A1=1.62, A2=2.13), and gene expression of SC, A1 and 2 were significantly increased in IUGR F21 brain (C=1.0, SC=1.64, A1=1.61, A2=2.15). No significant difference existed between C and IUGR gene expression in J4 animals, though by J14 a trend towards decreased expression of all four enzymes existed (C=1.0, ND4=0.83, SC=0.65, A1=0.82, A2=0.64). In J21 animals, cerebral gene expression of all four enzymes significantly declined in IUGR pups ≅50% relative to controls (C=1.0, ND4=0.41, SC=0.62, A1=0.49, A2=0.52). We conclude that alterations in the intrauterine milieu associated with placental insufficiency increase gene expression of ND4,SC,A1, and A2 despite sparing of gross brain growth. We speculate that increased fetal cerebral gene expression of these mitochondrial enzymes may predispose the IUGR infant to perinatal neurological damage and are a consequence of limited metabolic fuel. Interestingly, gene expression of all four mitochondrial enzymes declined in the IUGR juvenile despite removal from the altered intrauterine enviroment. A possible relationship between decreased cerebral mitochondrial gene expression and neurodevelopmental function requires future study.