Skip to main content
Dryad

Sleep deprivation drives brain-wide changes in cholinergic pre-synapse abundance in Drosophila melanogaster

Weiss, Jacqueline1; Blundell, Mei1; Singh, Prabhjit1; Donlea, Jeffrey1

Research facility: University of California, Los Angeles
Published Mar 11, 2024 on Dryad. https://doi.org/10.5061/dryad.q573n5tqv

Data files

Mar 11, 2024 version files 2.41 GB

Abstract

Sleep is an evolutionarily conserved state that supports brain functions, including synaptic plasticity, in species across the animal kingdom. Here, we examine the neuroanatomical and cell-type distribution of pre-synaptic scaling in the fly brain after sleep loss. We previously found that sleep loss drives accumulation of the active zone scaffolding protein Bruchpilot (BRP) within cholinergic Kenyon cells of the Drosophila melanogaster mushroom body (MB), but not in other classes of MB neurons. To test whether similar cell-type specific trends in plasticity occur broadly across the brain, we used an flp-based genetic reporter to label pre-synaptic BRP in cholinergic, dopaminergic, GABAergic, or glutamatergic neurons. We then collected whole-brain confocal image stacks of BRP intensity to systematically quantify BRP, a marker of pre-synapse abundance, across 37 neuropil regions of the central fly brain. Our results indicate that sleep loss, either by overnight (12h) mechanical stimulation or chronic sleep disruption in insomniac mutants, broadly elevates cholinergic synapse abundance across the brain, while synapse abundance in neurons that produce other neurotransmitters undergoes weaker, if any, changes. Extending sleep deprivation to 24 hours drives brain-wide upscaling in glutamatergic, but not other, synapses. Finally, overnight male-male social pairings induce increased BRP in excitatory synapses despite male-female pairings eliciting more waking activity, suggesting experience-specific plasticity. Within neurotransmitter class and waking context, BRP changes are similar across the 37 neuropil domains, indicating that similar synaptic scaling rules may apply across the brain during acute sleep loss and that sleep need may broadly alter the excitatory-inhibitory balance in the central brain.