Human and animal behaviour is determined by a range of factors, including environmental influences and biological differences in brain function. Individual trait differences in brain mechanisms lead to differences in psychological processing, ultimately producing differences in behaviour. Examples include the ability of cues that have previously (and may still) predict rewards in the environment to either attract and command attention (e.g. through a trait known as 'sign-tracking') or to control behaviour (as is the case with habitual or compulsive behaviour). Habits can be adaptive, allowing behaviour to proceed automatically with minimal cognitive effort and producing often-appropriate behaviour in the absence of conscious awareness. However, habits can become maladaptive if they become compulsive, 'must do' repetitive urges out of the individual's control. This occurs in many mental health disorders, including Obsessive-Compulsive Disorder (OCD) and drug addiction, but not all compulsive behaviours lead to a mental health disorder diagnosis. Compulsivity, like many psychological phenotypic traits, is on a continuum. We hypothesise that similar mechanisms underlie compulsivity across the spectrum, ranging from normal/adaptive to the maladaptive behaviour observed in mental health conditions. Furthermore, we hypothesise that these mechanisms, and the phenotypic traits that associate with habit formation and compulsivity, are conserved across species. Understanding the factors that influence the likelihood of once-adaptive habits becoming maladaptive and compulsive is important from the perspective of understanding fundamental learning processes. This project aims to test these hypotheses empirically in humans and rats, using our fully translational, rat-to-human Observing Response Task (ORT) to exploit the strengths of studies in each species. It is already known that in humans, attributing high levels of attention and value to reward-related cues ('sign-tracking') correlates with self-report of compulsive behaviours on questionnaires, and our previous work in rats has shown that sign-tracking is associated with compulsive-like checking behaviour on the ORT. However, the reliance on self-report measures in humans limits comparability to the rodent behavioural data. If we are to test whether the same mechanisms relate sign-tracking, habit formation and compulsivity in humans and animals, then we need to test empirically whether sign-tracking in humans is associated with objective behavioural measurements of repetitive behaviour, such as in the human version of the ORT. Furthermore, we need to know whether repetitive behaviours measured by the ORT are maladaptive and compulsive, and if the propensity to attribute high incentive value to reward-related cues leads to habit formation and compulsivity. These experiments will clarify, across species, the relationship between individual differences in the appetitive motivational system and the development of habitual (and sometimes maladaptive) behaviour. Using multiple behavioural measures, in addition to self-report (humans), specific lab-based translational behavioural tasks (humans and rats) and psychopharmacological studies (rats), we can determine how individual differences influence habitual and compulsive behaviour along the continuum of adaptive to maladaptive behaviour, and whether these trait differences directly drive habit formation and compulsivity. This will allow us to bridge the translational gap in studies of compulsive behaviour, which often rely upon self-report in humans and ethological measures in rodents.