Background: Our previous work has shown that the offspring of obese rat dams display an exaggerated and prolonged leptin surge early in life, which may predispose them to the metabolic syndrome in adulthood. It is hypothesized that this surge of leptin influences reward behaviour and the expression of associated receptors (e.g. dopamine D2, cannabinoid CB1 and opioid Mu receptors) in the central nervous system, Objective: This project investigated the ways in which elevated leptin levels in early life, comparable to those associated with maternal obesity, may alter the neonatal brain and lead to dysfunctional reward-seeking behaviours and obesity later in life. Methods: Twelve male Sprague Dawley rats were treated ip from post natal day 9-15 day with either leptin (0.3mg/kg, n=6) or vehicle (saline, n=6). At day 30, rats were euthanised and brains were removed for examination of receptor levels via ligand-binding autoradiography. An overnight ‘two-bottle sucrose preference test’ was also carried out in separate cohorts (n=10/group) at day 30. Results: Following an overnight sugar preference test, it was found that the leptin-treated rats had a greater preference for sucrose compared to the saline-treated control animals (94.6% vs. 84.7% preference for sucrose, p<0.05).Analysis of [3H]-spiperone binding indicated that the leptin treated-rats had a significantly lower D2 level than the control animals in the nucleus accumbens (64.8% lower, p<0.05); for CB1 binding, the leptin treatment led to a rise in the nucleus accumbens and decrease in the caudate putamen (p<0.05). Opioid mu receptor binding was higher in the nucleus accumbens and thalamus of the leptin-treated rats (p<0.05). Conclusions: Early-life leptin exposure leads to alterations in reward-related receptors and behaviour, which may predispose those individuals to reward-related behavioural disorders later in life, such as obesity or addiction.