Sleep restores behavioral plasticity to Drosophila mutants.

Sleep restores behavioral plasticity to Drosophila mutants.
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DOI:
10.1016/j.cub.2015.03.027
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发表时间:
2015-05-18
期刊:
影响因子:
9.2
通讯作者:
Shaw, Paul J.
Shaw, Paul J.
中科院分区:
生物学1区
文献类型:
--
作者:
Dissel, Stephane;Angadi, Veena;Kirszenblat, Leonie;Suzuki, Yasuko;Donlea, Jeff;Klose, Markus;Koch, Zachary;English, Denis;Winsky-Sommerer, Raphaelle;van Swinderen, Bruno;Shaw, Paul J.

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鉴于睡眠在调节可塑性方面所发挥的作用,我们假设增加睡眠可以恢复典型记忆突变体的记忆,而无需专门挽救因果性分子损伤。使用三种独立的策略增加睡眠:激活背侧扇形体(FB),增加脂肪酸结合蛋白(dFabp)的表达或通过给予GABA-A激动剂4,5,6,7-四氢异恶唑并[5,4-c]吡啶-3-醇(THIP)。利用厌恶趋光性抑制(APS)和求偶条件反射对芜菁甘蓝(rut)和邓塞(dnc)突变体的短时记忆(STM)或长时记忆(LTM)进行了评价。三种独立的策略都能增加rut和dnc突变体的睡眠和恢复记忆。重要的是,诱导睡眠还可以逆转阿尔茨海默病果蝇模型的记忆缺陷。总之,这些数据表明,睡眠在调节行为可塑性方面发挥着比以前更重要的作用,并表明增加睡眠可能对某些神经系统疾病患者有益。
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 (FB), 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 (APS) 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 suggests that increasing sleep may benefit patients with certain neurological disorders.
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