Sleep is an essential biological need that is regulated by multiple brain networks. The hypothalamus is a structure that is essential for the maintenance of physiological homeostasis including food intake, reproduction and sleep-wake states. The lateral hypothalamic area (LH) encompasses various cell groups critical for the coordination of arousal and REM sleep. In contrast, the preoptic area (POA) of the anterior hypothalamus is involved in the NREM sleep regulation. The predominant concept is that hypothalamic cells that govern sleep-wake states are clustered into wake-on, NREM-on or REM-on clusters. However, it remains unclear whether these clusters are functionally stable across the sleep-wake cycle, sleep homeostasis and sleep medication.In this study, we longitudinally recorded the single cell activity of different sub-populations of previously identified wake- and sleep-promoting neurons in LH and POA (LHVglut2, LHVgat，LHHcrt/OX, LHMCH and POAVgat )，respectively，using in vivo calcium imaging in free-behaving mice. We categorized and tracked neuron activity across sleep states as well as across sleep deprivation. The effect of a sleep medication, benzodiazepine (DZP), on the stability of POAVgat was also investigated. We found that while the number of state-dependent functional populations remained stable, a significant portion of individual neurons shifted between categories at different times of the day. SD could not evidently disturb neuron stability, however, DZP changed both single cell state selectivity and neuron population stability in a time-dependent manner. These results underscore the dynamic nature of neuronal encoding of sleep-wake within the hypothalamus and revisit the cellular underpinnings of sleep regulation.