From the start of the project, we investigated how visual attention and learning mechanisms assign priority to objects in complex environments, with a particular focus on incentive salience and its neural implementation. Early work established that visual attention is structured around objects, demonstrating with EEG that task-irrelevant object boundaries systematically shape anticipatory attentional deployment in human visual cortex, resolving longstanding ambiguity in behavioural accounts of object-based selection. This provided a mechanistic foundation for understanding how visual systems define candidate units for learning and value assignment.
Subsequent phases focused on how incentive salience is acquired, expressed, and suppressed for real-world object categories. Using machine-learning analysis of EEG and event-related potentials during naturalistic visual search, we showed that objects associated with reward rapidly acquire incentive salience, altering early sensory encoding. Critically, however, humans can also exert fast, stimulus-triggered suppressive control over incentive salience when reward-associated objects are known to be irrelevant. This suppression degrades neural representations of reward-associated distractors within ~200 ms, preventing attentional capture while preserving behavioural goal performance.
Together, these results demonstrate that incentive salience operates directly on visual representations and is dynamically regulated by cognitive control. This reframes reinforcement learning in vision as an object-centred process in which learned value reshapes perceptual encoding itself, rather than acting solely at post-perceptual decision stages. The findings imply that visual reinforcement learning involves continuous negotiation between value-driven incentive salience and top-down suppression.
Clinically, this has direct implications for addiction research. Maladaptive incentive salience attributed to drug-associated cues is a core feature of substance-use disorders, driving craving, attentional bias, and relapse. Our results identify rapid neural suppression of incentive salience as a candidate protective mechanism and a potential treatment target. By characterising when and how incentive salience can be overridden in visual cortex, this work provides a principled framework for developing biomarkers of vulnerability and for designing interventions that strengthen control over pathological incentive salience in addiction and related compulsive disorders.
Results have been disseminated in 20 journal articles, a variety of conference presentations and proceedings, and dozens of conference posters.
