Non-motor symptoms, such as sleep problems, often precede motor symptoms in patients with Parkinson’s Disease (PD). Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is used to control motor fluctuations of PD and there is increasing evidence that STN-DBS improves patients’ subjective sleep quality. However, how and if the STN regulates the sleep-wake cycle is unknown. We recorded activity of Vglut2-neurons in the STN during mice’s inactive period (lights on) and found peak calcium signals increased when mice transitioned from NREM to wake (p<0.05) and from NREM to REM (p<0.01, n=4) while signals decreased from wake to NREM (p<0.01) and REM to wake (p<0.01, n=4). Chemogenetic activation of STN vglut2-neurons with hM3Dq DREADD receptors induced wake and supressed NREM (p<0.01) and REM sleep (p<0.05, n=4), lasting for 5 hours post-CNO injection (1mg/kg, i.p.). However, unilateral deletion of STN Vglut2-neurons also increased wake (p<0.05) and reduced NREM and REM sleep (p<0.05, n=6) without affecting gross locomotor activity, suggesting there are subtypes of STN Vglut2 cells. Vglut2-neurons in the STN project to various regions, including the entopeduncular nucleus (EP), global pallidus, subtantia nigra pars reticulata and ventral pallidum. As deletion of Vglut2-neurons in the EP reduced REM sleep duration (p<0.001, n=10), and retrograde tracing of EP Vglut2-neurones showed the STN as a major excitatory target upstream, we hypothesised that a specific subset of EP-projecting STN Vglut2-neurones regulate REM sleep. Further understanding of the STN cellular subtypes and their corresponding function will allow opportunities for future target refinement of STN-DBS.