The Roles of Discrete Populations of Neurons Expressing Short Neuropeptide F in Sleep Induction in Drosophila melanogaster.

Sleep is of vital importance in our lives, yet we are far from understanding the neuronal networks that control the amount and timing of sleep. There is substantial conservation of known sleep-regulating transmitters, allowing for studies in simpler organisms to lead the way in gaining insight into the organization of sleep control circuits. In Drosophila melanogaster, we recently showed that optogenetic activation of neurons that produce the neuropeptide Y (NPY)-related transmitter short neuropeptide F (sNPF) increases time spent asleep. However, sNPF is expressed in several neuronal populations, and thus it is unknown which of those populations play roles in the sleep-promoting effect. In this study, we addressed this issue using a genetic approach to limit optogenetic activation to subsets of sNPF-expressing neurons. We found that sleep promotion was shorter-lived when cryptochrome (CRY)-positive neurons were excluded from being activated. Pigment-dispersing factor (PDF) neurons were not required for sleep promotion, nor were mushroom body (MB) neurons. Acute reactions to a short, 10-s period of optogenetic activation were largely unchanged by excluding activation of the three neuronal populations mentioned above. Together, these results suggest that clock neurons that are CRY-positive and PDF-negative are important contributors to the long-lasting sleep promotion produced by sNPF neuron activation. However, other neurons targeted by the sNPF-GAL4 driver appear to mediate the more rapid behavioral responses. Future studies will seek to identify these additional sNPF neuron populations and to determine how sNPF-expressing clock neurons act in concert with other neuronal circuits to promote sleep.