Dopaminergic neurons in the brain affect all stages of vigilance but the exact mechanisms of this regulation are poorly understood. The D1-dopamine receptor mediates behavioural arousal, while D2R activation induces biphasic effects: somnolence at low, waking at higher doses. Histaminergic neurons located in the tuberomamillary nucleus (TMN) of the posterior hypothalamus are wake-on pacemaker neurons controlling cortical arousal. We demonstrate that D2-like receptors are expressed in TMN neurons. D2-,D3- and D4-receptor activation increases TMN neurons firing rate. We tested the role of histamine in quinpirole induced behavioural arousal with the help of histidine decarboxylase knockout mice. Quinpirole dose-dependently (1, 5, 15, 30 mg/kg) enhanced waking upon i.p. injection. The lowest dose increased waking and suppressed slow wave sleep (SWS) in WT, but not in HDC KO mice. Higher doses of quinpirole suppressed REM (rapid eye movement) sleep to a larger extent in KO than in WT mice. In conclusion, the histaminergic system is activated through D2-like receptors and participates in dopamine-induced arousal.