It is believed that drugs of abuse usurp neural circuitry that initially evolved to mediate behavioral processes essential for fitness. Therefore, the takeover of this circuitry by drugs of abuse usually exerts powerful control over the behavior and this is a tremendous problem for many humans. One important factor affecting drug abuse is social environment. It has been shown that social attachments formed in adulthood may have significant, protective effects from drug addictions. However, investigation into this topic is limited partially because the vast majority of addiction research has been conducted on traditional laboratory rodent species such as rats and mice that do not form adult-adult social attachments. Here we propose a novel line of research to use a recently developed drug intravenous self-administration paradigm in a unique animal model and to address fundamental questions regarding the effects of social bonding and the role of neuropeptide oxytocin (OT) on drug reinstatement. The socially monogamous prairie vole (Microtus ochrogaster) displays mating-induced pair bonding between mates, and thus has been utilized as a premier rodent model for studying adult social bonding and its underlying neurochemical mechanisms. Recently it has been demonstrated that psychostimulant drug amphetamine (AMPH) and cocaine are rewarding to prairie voles as they induced conditioned place preference (CPP). It has also been shown that exposure to AMPH impaired pair bonding and pair bonding experience decreased the rewarding value of AMPH. Furthermore, neurochemicals such as dopamine (DA) and OT, which have been implicated in pair bonding behavior, are also involved in regulating drug and social behavior interactions. These data support the notion that natural reward and maladaptive drug reward are both regulated by overlapping neural mechanisms. These data also indicate the utility of the prairie vole model for this line of research. We have recently developed a cocaine intravenous self-administration paradigm in prairie voles, and we propose here to use this paradigm to further establish the prairie vole model for drug addiction research. In Specific Aim 1, we will examine whether social bonding with a partner will dampen or completely inhibit reinstatement to cocaine. In Specific Aim 2, we will investigate whether the neuropeptide OT in a particular brain region, the nucleus accumbens (NAcc), is able to reduce or block reinstatement to cocaine. Successful completion of these studies will further our understanding of behavioral and neurobiological interactions between social and drug rewards. Importantly, it will further establish a much needed rodent model to study the interaction between drug addiction and social bonding as well as its underlying neurochemical mechanisms, which, in turn, will have the potential to facilitate behavioral and neuropharmacological interventions that may aid with addiction extinction and prevention of relapse.