AbstractSleep is vital for survival. Yet, under environmentally challenging conditions such as starvation, animals suppress their need for sleep. Interestingly, starvation-induced sleep loss does not evoke a subsequent sleep rebound. Little is known about how starvation-induced sleep deprivation differs from other types of sleep loss, or why some sleep functions become dispensable during starvation. Here we demonstrate that downregulation of unpaired-2 (upd2, the Drosophila ortholog of leptin), is sufficient to mimic a starved-like state in flies. We use this ‘genetically starved’ state to investigate the consequences of a starvation signal on visual attention and sleep in otherwise well-fed flies, thereby sidestepping the negative side-effects of undernourishment. We find that knockdown of upd2 in the fat body is sufficient to suppress sleep while also increasing selective visual attention and promoting night-time feeding. Further, we show that this peripheral signal is integrated in the fly brain via insulin-expressing cells. Together, these findings identify a role for peripheral tissue-to-brain interactions in the simultaneous regulation of sleep and attention, to potentially promote adaptive behaviors necessary for survival in hungry animals.Author SummarySleep is important for maintaining both physiological (e.g., metabolic, immunological, and developmental) and cognitive processes, such as selective attention. Under nutritionally impoverished conditions, animals suppress sleep and increase foraging to locate food. Yet it is currently unknown how an animal is able to maintain well-tuned cognitive processes, despite being sleep deprived. Here we investigate this question by studying flies that have been genetically engineered to lack a satiety signal, and find that signaling from fat bodies in the periphery to insulin-expressing cells in the brain simultaneously regulates sleep need and attention-like processes.
The brain timewise: how timing shapes and supports brain function
