Dopamine inhibits neurons from the rat dorsal subcoeruleus nucleus through the activation of α2-adrenergic receptors.

Previous studies have revealed that the central dopaminergic system may participate in regulating sleep/wakefulness. In particular, rapid eye movement (REM) sleep behavior disorder (RBD) occurs in patients with Parkinson's disease (PD), highlighting the possible connection between dopamine and REM sleep-related neural structures. The dorsal subcoeruleus nucleus (SubCD) is a critical structure for the generation and maintenance of REM sleep. Thus, the present study investigated the modulatory effects of dopamine on SubCD neurons. Using whole-cell patch clamp recordings, we first observed that dopamine induced a hyperpolarization of the membrane potentials in SubCD neurons and thus inhibited their firing. We determined that a dose-dependent and tetrodotoxin-resistant postsynaptic outward current underpinned this inhibitory effect on SubCD neurons induced by dopamine. Finally, using pharmacological agents, we revealed that the dopamine-elicited outward current in SubCD neurons was mediated by α2-adrenergic receptors, but not by the dopamine receptors, including D1-like and D2-like receptors. These results suggest that the central dopaminergic system may play a role in the regulation of REM sleep through the effect of dopamine on SubCD neurons. The relationship between the loss of this effect and the RBD in PD is discussed.