| Literature DB >> 25913403 |
Stephane Dissel1, Veena Angadi1, Leonie Kirszenblat2, Yasuko Suzuki1, Jeff Donlea3, Markus Klose1, Zachary Koch1, Denis English1, Raphaelle Winsky-Sommerer4, Bruno van Swinderen2, Paul J Shaw5.
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.Entities:
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Year: 2015 PMID： 25913403 PMCID： PMC4465363 DOI： 10.1016/j.cub.2015.03.027
Source DB: PubMed Journal: Curr Biol ISSN： 0960-9822 Impact factor: 10.834