Single nuclei RNA sequencing unmasks 16 variants of midbrain dopamine neurons within a continuum of their gene expression landscape and resolves their differential vulnerability.

Midbrain dopamine neurons function according to their axonal projections in the intact brain.

Regulation of Cav2.3 Ca²⁺ channels by membrane-bound β2 subunit splice variants permits long-lasting channel activity even during prolonged and continuous activity in dopamine neurons, with implications for Parkinson's disease pathophysiology.

APEX2 proximity labeling of genetically targeted neurons enables subcellular and cell type-specific proteomics in the mouse brain, revealing the axonal and somatodendritic proteomes of midbrain dopaminergic neurons.

Dopamine signaling is necessary for normal fear extinction learning.

Frontal cortical circuit alterations and cognitive deficits identified in mouse genetic models are reversed by chemogenetic or optogenetic stimulation of the mesocortical dopamine circuit in an adolescent period.

The midbrain area for salience, reward and aversion in mouse brain harbours among the dopamine cells three subtypes somatostatin-expressing neurons that show combinatorial neurotransmitter phenotypes and interneuron properties.

Promoting a Warburg-like shift in astrocytic metabolism through reduced mitochondrial electron transport accommodates the energetic burden caused by brain trauma without overwhelming cellular respiration and redox to salvage dopaminergic neurons.

Genetic analysis of Ntn1 in adult mouse midbrain neurons reveals its function in maintaining excitatory synapses, loss of Ntn1 function in inhibitory neurons is significantly detrimental to mesolimbic system function.

Despite the fundamental relationship between movement and value, they are represented in a separable manner in dopamine neurons.