Abstract
SummarySleep-promoting neurons in the dorsal fan-shaped body (dFB) of Drosophila are integral to sleep homeostasis, but how these cells impose sleep on the organism is unknown. We report that dFB neurons communicate via inhibitory transmitters, including allatostatin-A (AstA), with interneurons connecting the superior arch with the ellipsoid body of the central complex. These “helicon cells” express the galanin receptor homolog AstA-R1, respond to visual input, gate locomotion, and are inhibited by AstA, suggesting that dFB neurons promote rest by suppressing visually guided movement. Sleep changes caused by enhanced or diminished allatostatinergic transmission from dFB neurons and by inhibition or optogenetic stimulation of helicon cells support this notion. Helicon cells provide excitation to R2 neurons of the ellipsoid body, whose activity-dependent plasticity signals rising sleep pressure to the dFB. By virtue of this autoregulatory loop, dFB-mediated inhibition interrupts processes that incur a sleep debt, allowing restorative sleep to rebalance the books.Video
Highlights
The behavioral hallmarks of sleep are manifold
The sleep-promoting neurons send projections to the dorsal fan-shaped body of the central complex and act as a feedback controller or homeostat (Donlea et al, 2014). Their operating principle is remarkably simple: sleep need is encoded in the intrinsic electrical excitability of the sleep-inducing cells, which fluctuates because two potassium conductances, voltage-gated Shaker and the leak channel Sandman, are modulated antagonistically (Donlea et al, 2014; Pimentel et al, 2016)
As sleep pressure builds during waking, the sleep-promoting neurons switch from electrical silence to activity and the animal from wakefulness to restorative sleep
Summary
The behavioral hallmarks of sleep are manifold. They include inactivity, reduced responsiveness to external stimuli, rapid reversibility, and homeostatic rebound after sleep loss. Any sleep control system must fulfill a multitude of functions— blocking locomotor activity, gating sensory pathways, inhibiting arousal systems, relieving sleep pressure—and perhaps directly influence processes germane to a fundamental purpose of sleep, be it metabolic recovery (Vyazovskiy and Harris, 2013; Walker et al, 1979), memory consolidation (Wilson and McNaughton, 1994), or synaptic scaling (Tononi and Cirelli, 2003). The sleep-promoting neurons send projections to the dorsal fan-shaped body (dFB) of the central complex and act as a feedback controller or homeostat (Donlea et al, 2014) Their operating principle is remarkably simple: sleep need is encoded in the intrinsic electrical excitability of the sleep-inducing cells, which fluctuates because two potassium conductances, voltage-gated Shaker and the leak channel Sandman, are modulated antagonistically (Donlea et al, 2014; Pimentel et al, 2016). The self-correcting nature of feedback is embodied in the biophysics of an excitability switch
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