Sleep deprivation results in diverse patterns of synaptic scaling across the Drosophila mushroom bodies.

Sleep deprivation results in diverse patterns of synaptic scaling across the Drosophila mushroom bodies.
复制标题

睡眠剥夺导致果蝇蘑菇体中突触缩放的不同模式。

DOI:
10.1016/j.cub.2021.05.018
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发表时间:
2021-08-09
期刊:
Current biology : CB
影响因子:
--
通讯作者:
Donlea JM
Donlea JM
中科院分区:
其他
文献类型:
--
作者:
Weiss JT;Donlea JM

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睡眠对包括学习和记忆在内的各种可塑性过程都是必不可少的。然而,睡眠不足对电路连通性的影响仍然知之甚少。为了更好地理解睡眠不足对跨越记忆编码电路的突触连接的影响,我们研究了突触标记在果蝇蘑菇体(MB)中分布的变化。活动区成分的蛋白质陷阱标签表明,最近的睡眠时间与MB叶中BruchPilot(BRP)的丰度成反比;睡眠不足会提高BRP,而睡眠诱导会降低MB中的BRP。夜间睡眠不足也会增加dSyd-1和杂音的水平,但不会增加其他突触前蛋白的水平。细胞类型特异性遗传报告显示,睡眠剥夺后,MB固有的Kenyon细胞(KCs)在整个轴突叶显示突触前BRP增加;在支配MB的大型中间神经元或多巴胺能神经元的投射中未检测到类似的增加。这些结果表明,KCs的突触前可塑性是睡眠剥夺果蝇MB叶BRP水平升高的原因。由于KC为几类突触后伙伴提供突触输入,我们接下来使用突触接触的荧光报告器来测试每类KC输出连接是否因睡眠缺失而统一缩放。我们在这里观察到的KC输出突触可以分为三类:KCS到MB中间神经元,KCs到多巴胺能神经元,KCs到MB输出神经元。没有一个单一的类别在每个组成成员上显示出统一的比例,这表明不同的规则可能控制着不同类型细胞在睡眠丧失期间的可塑性。Weiss和Donlea发现,睡眠不足增加了突触前Bruchilot穿过果蝇蘑菇体(MB),这是由于MB固有的Kenyon细胞的可塑性。从Kenyon细胞到突触后靶点的接触显示出随着睡眠减少而发生的不同变化,这表明睡眠剥夺可能会不同地改变不同类别的MB突触。
Sleep is essential for a variety of plastic processes, including learning and memory. However, the consequences of insufficient sleep on circuit connectivity remain poorly understood. To better appreciate the effects of sleep loss on synaptic connectivity across a memory-encoding circuit, we examined changes in the distribution of synaptic markers in the Drosophila Mushroom body (MB). Protein-trap tags for active zone components indicate that recent sleep time is inversely correlated with Bruchpilot (BRP) abundance in the MB lobes; sleep loss elevates BRP while sleep induction reduces BRP across the MB. Overnight sleep deprivation also elevated levels of dSyd-1 and Cacophony, but not other pre-synaptic proteins. Cell-type specific genetic reporters show that MB-intrinsic Kenyon cells (KCs) exhibit increased pre-synaptic BRP throughout the axonal lobes after sleep deprivation; similar increases were not detected in projections from large interneurons or dopaminergic neurons that innervate the MB. These results indicate that pre-synaptic plasticity in KCs is responsible for elevated levels of BRP in the MB lobes of sleep-deprived flies. Because KCs provide synaptic inputs to several classes of post-synaptic partners, we next used a fluorescent reporter for synaptic contacts to test whether each class of KC output connections is scaled uniformly by sleep loss. The KC output synapses that we observed here can be divided into three classes: KCs to MB interneurons, KCs to dopaminergic neurons, and KCs to MB output neurons. No single class showed uniform scaling across each constituent member, indicating that different rules may govern plasticity during sleep loss across cell types. Weiss and Donlea find that sleep loss increases pre-synaptic Bruchpilot across the Drosophila Mushroom Body (MB) due to plasticity in MB-intrinsic Kenyon cells. Contacts from Kenyon cells to post-synaptic targets show differing changes with sleep loss, indicating that sleep deprivation may differentially alter distinct classes of MB synapses.
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