In rodents and primates, there are two subtypes of parvalbumin-expressing interneurons that provide novel substrates for selective inhibition in the striatum.
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.
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.
By differentially modulating the two major excitatory inputs to the striatum, mu- and delta-opioid receptors regulate the balance between thalamic and cortical inputs to the striatum.
Computational modeling suggests that feedback between striatal cholinergic neurons and spiny neurons dynamically adjusts learning rates to optimize behavior in a variable world.
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.
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.
Behavioral, pharmacological, optogenetic, electrophysiological and computational analyses suggest that the anterior dorsal striatum is a causal node in the network responsible for evidence accumulation.
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.