Recent success in training artificial agents and robots derives from a combination of direct learning of behavioral policies and indirect learning via value functions. Policy learning and value learning employ distinct algorithms that depend upon evaluation of errors in performance and reward prediction errors, respectively. In mammals, behavioral learning and the role of mesolimbic dopamine signaling have been extensively evaluated with respect to reward prediction errors; but there has been little consideration of how direct policy learning might inform our understanding. I’ll discuss our recent work on classical conditioning in naïve mice (https://www.biorxiv.org/content/10.1101/2021.05.31.446464v1) that provides multiple lines of evidence that phasic dopamine signaling regulates policy learning from performance errors in addition to its well-known roles in value learning. This work points towards new opportunities for unraveling the mechanisms of basal ganglia control over behavior under both adaptive and maladaptive learning conditions.

Transient changes in dopamine activity in response to reward and punishment have been known to regulate reward-related learning. However, the cellular basis that detects the transient dopamine signaling has long been unclear. Using two-photon microscopy and optogenetics, I have shown that transient increases and decreases of dopamine modulate plasticity of dopamine D1 and D2 receptor-expressing cells in the nucleus accumbens, respectively. At the behavioral level, I characterized that these D1 and D2 cells cooperatively tune learning by generalization and discrimination learning. Interestingly, disturbance of the dopamine signaling impaired D2 cell plasticity and discrimination learning, which was analogous to salience misattribution seen in subjects with schizophrenia.