The development of the electrical phenotype of neurons can be precisely quantified and dissected using a combination of multi-variate statistical analyses and a systematic electrophysiological characterization of electrical properties.

The human substantia nigra can be parcellated into three subdivisions that subserve emotional, cognitive and somatomotor function.

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

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.

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.

The first comprehensive insight into speed, trajectory and morphology profiles of tangentially migrating dopaminergic neurons and the alterations in their migratory behavior in absence of Reelin signaling.

The transition in basal ganglia output from the healthy to the diseased state is biphasic, stereotyped across models, and suggests key time points for delivering therapeutic interventions.

Dopaminergic cells uniquely receive input from a roughly equal mixture of synapses on dendritic spines and synapses formed directly on dendrites.

The sodium leak NALCN channel functions as a core effector of GABA-B and D2 receptors that is used along with GIRK channels to regulate action potential firing in dopamine neurons.

The pattern of atrophy in Parkinson's disease is consistent with the disease spreading via intrinsic brain networks.