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 alpha(2)-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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.