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 effects of chloride homeostasis can explain diverse responses of basal ganglia output neurons to putatively inhibitory inputs and may tune these neurons' synchrony, oscillations and behavior in decision-making scenarios.
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.
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.
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.
