Abstract
Sleep is an important body state that is widely conserved across the animal kingdom. Given the fact that sleepless animals have not been found on earth, and that sleep deprivation is harmful to animals, the reason why sleep is necessary still remains a mystery. In a previous study, the “synaptic homeostasis hypothesis” (SHY) was proposed as an explanation, which argues that sleep down-regulates the global synaptic strength by either reducing synapse number or depressing synaptic connectivity, while wakefulness increases synaptic strength when animals are exposed to the changing environment. In other words, sleep serves to maintain homeostatic regulation, without which the animal brain would be saturated by the increasing amount of synapses.\r Sleep need is regulated by the circadian rhythm of an animal as well as sleep pressure. In Drosophila melanogaster, sleep pressure is regulated by a plastic change within a subset of ellipsoid body (EB) neurons, who communicate with anterior- projecting dorsal neurons (APDN) In this study, we tested the effect of sleep on synapses. We used several methods to \r observe the distribution of a synaptic protein, Bruchpilot (BRP) in two sets of circadian neurons that directly regulate the morning and evening peak of flies. We found that sleep cycles had no observable effect on the synaptic strength. However, optogenetic activation of the sleep-inducing DN1 neurons using CsChrimson led to a dramatic increase in BRP levels in dorsal processes of DN1s. We therefore suggest that it is neuronal activation rather than the wake/sleep stage of the animal that regulates synaptic strength.