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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.

Original publication

DOI

10.1016/j.cub.2015.03.027

Type

Journal article

Journal

Curr Biol

Publication Date

18/05/2015

Volume

25

Pages

1270 - 1281

Keywords

Adenylyl Cyclases, Alzheimer Disease, Animals, Animals, Genetically Modified, Behavior, Animal, Disease Models, Animal, Drosophila Proteins, Drosophila melanogaster, Fatty Acid-Binding Proteins, Female, Isoxazoles, Male, Memory, Long-Term, Memory, Short-Term, Mutation, Organophosphorus Compounds, Receptors, GABA, Reserpine, Sleep