Sleep Restores Behavioral Plasticity to Drosophila Mutants

Dissel, Stepane, Angadi, Veena, Kirszenblat, Leonie, Suzuki, Yasuko, Donlea, Jeff, Klose, Markus, Koch, Zachary, English, Denis, Winsky-Sommerer, Raphaelle, van Swinderen, Bruno and Shaw, Paul J. (2015) Sleep Restores Behavioral Plasticity to Drosophila Mutants. Current Biology, 25 10: 1270-1281. doi:10.1016/j.cub.2015.03.027


Author Dissel, Stepane
Angadi, Veena
Kirszenblat, Leonie
Suzuki, Yasuko
Donlea, Jeff
Klose, Markus
Koch, Zachary
English, Denis
Winsky-Sommerer, Raphaelle
van Swinderen, Bruno
Shaw, Paul J.
Title Sleep Restores Behavioral Plasticity to Drosophila Mutants
Journal name Current Biology   Check publisher's open access policy
ISSN 0960-9822
1879-0445
Publication date 2015-01-01
Year available 2015
Sub-type Article (original research)
DOI 10.1016/j.cub.2015.03.027
Open Access Status Not yet assessed
Volume 25
Issue 10
Start page 1270
End page 1281
Total pages 12
Place of publication Cambridge, MA United States
Publisher Cell Press
Language eng
Subject 1300 Biochemistry, Genetics and Molecular Biology
1100 Agricultural and Biological Sciences
Abstract Given the role that sleep plays in modulating plasticity, we hypothesized that increasing sleep would restore memory to canonical memory mutants without specifically rescuing the causal molecular lesion. Sleep was increased using three independent strategies: activating the dorsal fan-shaped body, increasing the expression of Fatty acid binding protein (dFabp), or by administering the GABA-A agonist 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP). Short-term memory (STM) or long-term memory (LTM) was evaluated in rutabaga (rut) and dunce (dnc) mutants using aversive phototaxic suppression and courtship conditioning. Each of the three independent strategies increased sleep and restored memory to rut and dnc mutants. Importantly, inducing sleep also reverses memory defects in a Drosophila model of Alzheimer's disease. Together, these data demonstrate that sleep plays a more fundamental role in modulating behavioral plasticity than previously appreciated and suggest that increasing sleep may benefit patients with certain neurological disorders.
Formatted abstract
Given the role that sleep plays in modulating plasticity, we hypothesized that increasing sleep would restore memory to canonical memory mutants without specifically rescuing the causal molecular lesion. Sleep was increased using three independent strategies: activating the dorsal fan-shaped body, increasing the expression of Fatty acid binding protein (dFabp), or by administering the GABA-A agonist 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP). Short-term memory (STM) or long-term memory (LTM) was evaluated in rutabaga (rut) and dunce (dnc) mutants using aversive phototaxic suppression and courtship conditioning. Each of the three independent strategies increased sleep and restored memory to rut and dnc mutants. Importantly, inducing sleep also reverses memory defects in a Drosophila model of Alzheimer’s disease. Together, these data demonstrate that sleep plays a more fundamental role in modulating behavioral plasticity than previously appreciated and suggest that increasing sleep may benefit patients with certain neurological disorders.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2016 Collection
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 29 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 27 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Tue, 05 May 2015, 14:58:11 EST by System User on behalf of Queensland Brain Institute