How the human brain generates conscious phenomenal experience is a fundamental problem. In particular, it is unknown how variable and dynamic changes in subjective affect are driven by interactions with objective phenomena. We hypothesize a neurocomputational mechanism that generates valence-specific learning signals associated with 'what it is like' to be rewarded or punished. Our hypothesized model maintains a partition between appetitive and aversive information while generating independent and parallel reward and punishment learning signals. This valence-partitioned reinforcement learning (VPRL) model and its associated learning signals are shown to predict dynamic changes in 1) human choice behavior, 2) phenomenal subjective experience, and 3) BOLD-imaging responses that implicate a network of regions that process appetitive and aversive information that converge on the ventral striatum and ventromedial prefrontal cortex during moments of introspection. Our results demonstrate the utility of valence-partitioned reinforcement learning as a neurocomputational basis for investigating mechanisms that may drive conscious experience.

In the mammalian brain, midbrain dopamine neuron activity is hypothesized to encode reward prediction errors that promote learning and guide behavior by causing rapid changes in dopamine levels in target brain regions. This hypothesis (and alternatives regarding dopamine's role in punishment-learning) has limited direct evidence in humans. We report intracranial, subsecond measurements of dopamine release in human striatum measured while volunteers (i.e., patients undergoing deep brain stimulation (DBS) surgery) performed a probabilistic reward- and punishment-learning choice task designed to test whether dopamine release encodes only reward prediction errors or whether dopamine release may also encode adaptive punishment-learning signals. Results demonstrate that extracellular dopamine levels can encode both reward and punishment prediction errors, but may do so via independent valence-specific pathways in the human brain.