Changes of Sleep-wake Behavior and Circadian Rhythmicity in a Mouse Model of Vitamin D Deficiency

Abstract

Vitamin D deficiency, which is prevalent in modern societies, is associated with an increased risk of developing diseases such as diabetes, heart diseases, autoimmune diseases, and cancers. Vitamin D deficiency has also been reported to be linked to sleep disturbances, such as reduced sleep duration and lower sleep quality, but the underlying mechanism is not understood yet. Vitamin D receptor (VDR) has been shown to be highly expressed in several subcortical nuclei, including, but not limited to, bed nucleus of the stria terminalis (BNST), thalamic reticular nucleus (TRN), dorsal raphe nucleus (DRN) and central nucleus of the amygdala (CeA). Interestingly these nuclei are also known to play essential roles in controlling the sleep-wake behavior. Given that VDR is robustly found in sleep-related regions in the brain, it is plausible that vitamin D deficiency may be implicated in the disturbances of sleep-wake control and circadian rhythm. However, there is a lack of biological evidence to support this causal relationship. Therefore, I hypothesized that vitamin D might play an essential role in controlling sleep-wake behavior and the circadian rhythmicity and sought to elucidate its neurobiological mechanism in an animal model of vitamin D deficiency.