Abstract
Genes and neural circuits coordinately regulate animal sleep. However, it remains elusive how these endogenous factors shape sleep upon environmental changes. Here, we demonstrate that Shaker (Sh)-expressing GABAergic neurons projecting onto dorsal fan-shaped body (dFSB) regulate temperature-adaptive sleep behaviors in Drosophila. Loss of Sh function suppressed sleep at low temperature whereas light and high temperature cooperatively gated Sh effects on sleep. Sh depletion in GABAergic neurons partially phenocopied Sh mutants. Furthermore, the ionotropic GABA receptor, Resistant to dieldrin (Rdl), in dFSB neurons acted downstream of Sh and antagonized its sleep-promoting effects. In fact, Rdl inhibited the intracellular cAMP signaling of constitutively active dopaminergic synapses onto dFSB at low temperature. High temperature silenced GABAergic synapses onto dFSB, thereby potentiating the wake-promoting dopamine transmission. We propose that temperature-dependent switching between these two synaptic transmission modalities may adaptively tune the neural property of dFSB neurons to temperature shifts and reorganize sleep architecture for animal fitness.
Highlights
Genes and neural circuits coordinately regulate animal sleep
Sleep behaviors are likely governed by more complex mechanisms in light:12-h dark (LD) cycles, our results demonstrate that light and temperature cooperatively gate the sleep-promoting effects of Sh in a manner independent of circadian rhythms or sleep homeostasis
While Resistant to dieldrin (Rdl) expression in dorsal fan-shaped body (dFSB) neurons has been reported previously[50,51,52], we found that dFSB-specific Rdl depletion lengthened wild-type long daytime sleep (L sleep) at 21 °C, but not at 29 °C (Fig. 4)
Summary
Genes and neural circuits coordinately regulate animal sleep. it remains elusive how these endogenous factors shape sleep upon environmental changes. We demonstrate that Shaker (Sh)-expressing GABAergic neurons projecting onto dorsal fan-shaped body (dFSB) regulate temperature-adaptive sleep behaviors in Drosophila. The SH complex represents one of the major sleep-promoting pathways in Drosophila, Shindependent sleep regulation by sss has been reported[10]. D1-like DA receptors, Dop1R1 and Dop1R2, transmit the inhibitory dopaminergic input to dFSB neurons and suppress their sleep-promoting neural activity[18,19,21]. Sleep need is further sensed by the elevation of mitochondrial reactive oxygen species and the subsequent oxidation of nicotinamide adenine dinucleotide phosphate bound to HK25 The latter leads to highfrequency spiking in dFSB neurons that induces sleep, underlying their role in sleep homeostasis
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