Leptin receptors (LR) mediate central (satiety) and peripheral metabolic actions of the translated and secreted product of the obese (ob) gene. While two isoforms as products of RNA splicing have been characterized, both of them bind leptin on the same epitope. Even though LR has been reported in adult tissues, limited information exists with respect to its presence and tissue-distribution in the embryo. We examined the spatial and temporal distribution of LR in the rat conceptus and placenta from d9 to d21 at 2 day intervals (term≈d21), and postnatal d15, and d30 (n=7/age/group). Employing frozen saggital embryonic and postnatal rat sections, 125I-leptin binding in the presence and absence of 0.6 × 10-6M unlabeled leptin was assessed by autoradiography and microdensitometry (Molecular Analyst Microdensitometry Program - 1.4.1, NIH). On d9, the placenta revealed LR while the known control (125I-insulin binding [IR]) was noted in amniotic membranes. At d11, LR was noted in the liver, while liver IR was present at d13. LR was present in the brain [d13], spine and long bones [d13], heart [d15], and kidney [d17]. The LR increased 2.5 fold in density from d9 to d21 (p < 0.01), with a subsequent 3-fold rise postnatally reaching a peak at d15 (p < 0.05). In contrast, IR demonstrated a 1.5-fold increase prenatally followed by a peak at postnatal d15. We conclude that 1] LR are present in embryonic tissues although the ontogenic peak is observed postnatally at d15, 2] LR are distributed in various tissues, with the earliest appearance being limited to the placenta and liver even before its appearance in the brain. We speculate that LR mediate the biological effects of leptin both centrally and peripherally in the embryo thereby regulating metabolism and growth.