Reward Valuation in Large Language Models: Causal Induction of Anhedonia

Recent frontier models mimic complex aspects of human cognition. Here we ask whether this alignment extends into reward valuation, which we assess in a mechanistic framework. Specifically, we use clinical tests that were developed to evaluate anhedonia in human subjects with major depressive disorders. Mechanistically, anhedonia is frequently associated with dysregulation in the Nucleus Accumbens (NAc) and the broader dopaminergic reward system. While neuroimaging has localized these deficits, establishing a causal link between NAc activity and specific behavioral symptoms remains a challenge. We use these ideas from neuroscience to functionally identify reward-anticipatory units in state-of-the-art AI models, and evaluate their causal involvement via targeted perturbations. We find that not only are such model units predictive of NAc brain recordings, their perturbation also induces behavioral effects mirroring human anhedonia: the model opts for low-effort, low-reward tasks in effort-based decision-making paradigms. Crucially, our results demonstrate that this represents a specific deficit in self-centered reward valuation and anticipation--rather than a loss of task capability, reward calculation, or effort avoidance. This induced vulnerability aligns with clinical measures of anhedonia and motivation in humans, such as DARS and MAP-SR, instruments that contain no reward-related vocabulary, ruling out a purely lexical account of the perturbation effect. Taken together, our results suggest reward valuation circuits in AI models that functionally mimic those in humans.