While the basal ganglia have long been thought to mediate learning through dopamine-dependent striatal plasticity, their regulation of motor thalamus plays an unexpected and critical role in reinforcement.

Dopamine neurons make novel glutamatergic connections to striatal cholinergic interneurons in the lateral dorsal striatum that are mediated by metabotropic glutamate receptors coupled to TrpC channels.

In rodents and primates, there are two subtypes of parvalbumin-expressing interneurons that provide novel substrates for selective inhibition in the striatum.

Behavioral, pharmacological, optogenetic, electrophysiological and computational analyses suggest that the anterior dorsal striatum is a causal node in the network responsible for evidence accumulation.

Rostral and central striatum controls slow-wave sleep during active phase in mice.

The first comprehensive map of all excitatory inputs to the mouse striatum is presented and used to define and demarcate striatal subdivisions, including a previous unappreciated novel subdivision in the posterior striatum.

Computational modeling suggests that feedback between striatal cholinergic neurons and spiny neurons dynamically adjusts learning rates to optimize behavior in a variable world.

Optical recordings reveal previously unknown neuromodulator dynamics in the striatum during animal movements that suggest a new interpretation of the underpinnings of bradykinetic movements exhibited in Parkinson's Disease patients.

Dopamine novelty signals are localized in the posterior tail of the striatum along with general salience signals, while dopamine in the ventral striatum reliably encodes reward prediction error.

The numerous reports in support of action-value representation in the striatum are based on statistical analyses that are subject to two critical confounds and, thus, this long-held belief of striatal action-value representation should be retested using different experiments and analyses.