HAL (France)
open access
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 d
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