Environmental cues predicting the arrival of specific rewards are used to govern adaptive behavior. For example, if you’re walking down the street and smell the aroma coming from a fast food restaurant, it may entice you to go in to order a burger. Drugs of abuse can hijack these learning pathways. Indeed, drug addiction is thought to be driven by drug-paired cues having increased control over behavior associated with drug seeking. It is unclear whether the increases in the ability of drug-paired cues to exert control over behavior is due to the repetitive action to consume the drug (creating aberrant learning of drug contingencies), or whether the drug itself sensitizes circuits involved in reward learning. To test this, we examined whether non-contingent methamphetamine would impact cue-governed reward-seeking. Rats first received experimenter-administered injections of methamphetamine (drug group) or saline (control group) according to a schedule determined by rats that had self-administered methamphetamine in prior experiments in our lab. Then, rats underwent a Pavlovian-to-instrumental (PIT) procedure. This involves first teaching rats that two cues (e.g. tone and click) lead to two different rewards (e.g. sucrose pellets and maltodextrin liquid). Subsequently, rats separately learned to press levers to obtain these rewards (e.g. left lever→pellet, right lever→liquid). Finally, we test what rats have learnt about these associations by playing the cues in a test phase, and examining how this influences lever-pressing behavior in the absence of reward feedback. Usually, rats will show that they have learnt the specific contingencies by increasing responding on the lever producing sucrose when the cue paired with sucrose is played. This shows that they have formed a sensory-specific association between the cue and sucrose, and lever and sucrose, and are using that information to guide adaptive behavior. However, rats given prior injections of methamphetamine show an enhancement in cue-invigorated lever-press responding for specific rewards. This demonstrates that methamphetamine promotes reward-paired cues to exert heightened control over behavior directed towards specific rewards, and that this is due to influences of the drug on the circuit rather than changes in drug-reward contingencies. Given recent findings for hypothalamic-midbrain circuitry in this form of reward learning, we are interested in further investigating whether this circuit underlies the effect of methamphetamine on cue control of behavior.