Deletion of the sodium leak channel NALCN in dopamine neurons alters D2R-mediated signalling and psychostimulant responsiveness.
Midbrain dopamine (DA)-neurons are slow pacemakers that continuously fire action potentials, maintaining basal extracellular DA levels in target regions. The sodium leak channel NALCN has been identified as a key contributor in the pacemaker control of these neurons. However, the consequences of a disrupted DA pacemake...