Gene manipulation combined with behavior analysis reveals a role of miR-9 in modulating basal-ganglia-dependent developmental vocal learning and adult vocal performance via regulating the FOXP1/FOXP2 gene network and dopamine signaling in songbirds.

Negative feedback signals within the substantia nigra regulate the output of the basal ganglia, with implications for disorders such as Parkinson's disease.

The spiking activity of the subthalamic nucleus, rather than the activity of striatal projection neurons, orchestrates basal ganglia downstream activity and output commands in health and Parkinson’s disease.

A model based on the architecture of basal ganglia and validated with behavior and neuroimaging distinguishes mechanisms of action cancellation from no-go decisions.

Activity in cortico-basal ganglia circuits of juvenile songbirds reflects evaluative signals necessary for comparing self-generated behavior to a goal representation during skill learning.

The basal ganglia may preferentially influence movements based on internal goals rather than those guided by external stimuli.

Patterns of coordinated activity in the basal ganglia predict how much force we will use to grip objects, suggesting that individuals with paralysis may ultimately be able to use these signals to control graded responses in robotic devices.

The most common inherited dystonia, DYT1, is likely caused primarily by the dysfunction of the cerebellum rather than the basal ganglia.

Basal ganglia output neurons use the NALCN leak channel to maintain their characteristic tonic firing, and this channel is important for the modulation of firing by metabolic or receptor-mediated signals.

Pedunculopontine neurons can evoke burst spiking in substantia nigra dopaminergic neurons without engaging a subtype of glutamate receptor previously thought to be necessary for this spiking mode.