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

成果类型:
Article
署名作者:
Weiss, Jacqueline T.; Blundell, Mei Z.; Singh, Prabhjit; Donlea, Jeffrey M.
署名单位:
University of California System; University of California Los Angeles; University of California Los Angeles Medical Center; David Geffen School of Medicine at UCLA; University of California System; University of California Los Angeles; University of California Los Angeles Medical Center; David Geffen School of Medicine at UCLA; University of California System; University of California Davis
刊物名称:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN/ISSBN:
0027-13502
DOI:
10.1073/pnas.2312664121
发表日期:
2024-03-26
关键词:
synaptic plasticity in-vivo neurons homeostasis bruchpilot excitation synapses balance need excitation/inhibition
摘要:
Sleep is an evolutionarily conserved state that supports brain functions, including synsimilar cell type-specific trends in plasticity occur broadly across the brain, we used a flp- based genetic reporter to label presynaptic 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 presynapse abundance, across 37 neuropil regions of the central fly brain. Our results indicate that sleep loss, either by overnight (12- h) 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 h 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 excitatory-inhibitory balance in the central brain.