Remembering and forgetting in sleep: Selective synaptic plasticity during sleep driven by scaling factors Homer1a and Arc.

Remembering and forgetting in sleep: Selective synaptic plasticity during sleep driven by scaling factors Homer1a and Arc.
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睡眠中的记忆和遗忘:睡眠期间由缩放因子 Homer1a 和 Arc 驱动的选择性突触可塑性。

DOI:
10.1016/j.ynstr.2022.100512
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发表时间:
2023-01
影响因子:
5
通讯作者:
Diering, Graham H.
Diering, Graham H.
中科院分区:
医学2区
文献类型:
--
作者:
Diering, Graham H.

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睡眠是支持学习和记忆的保守和必要的过程。突触是睡眠功能的主要目标,也是睡眠需求的所在地。文献中的证据表明,睡眠的需要具有细胞或微电路水平的基础,并且睡眠需要可以在局部脑区域内积累,作为清醒活动的函数。睡眠促进激酶的激活和突触磷酸化的积累最近被证明是局部睡眠需要的分子基础的一部分。该领域的一个突出假设表明,睡眠的一些益处是由睡眠期间突触强度的广泛但选择性的减弱或按比例缩小介导的,以抵消清醒期间突触增强引起的兴奋性增加。文献还表明,突触可以在睡眠期间得到加强,这就提出了一个问题,即什么样的分子机制可以允许在睡眠期间选择突触可塑性类型。在这里,我描述了比例因子Arc和Homer1a在选择性可塑性中的作用机制以及与睡眠需求的联系。Arc和Homer1a在神经元中响应于清醒的神经元活动而被诱导,并随着清醒时间的推移而积累。我认为,在睡眠期间,弧和Homer1a驱动广泛削弱突触通过稳态缩小,但在某种程度上是敏感的可塑性历史的个别突触,基于模式化的磷酸化突触蛋白。因此,Arc和Homer1a可能会对睡眠需求的细胞基础和睡眠期间记忆巩固之间的复杂联系提供见解。
Sleep is a conserved and essential process that supports learning and memory. Synapses are a major target of sleep function and a locus of sleep need. Evidence in the literature suggests that the need for sleep has a cellular or microcircuit level basis, and that sleep need can accumulate within localized brain regions as a function of waking activity. Activation of sleep promoting kinases and accumulation of synaptic phosphorylation was recently shown to be part of the molecular basis for the localized sleep need. A prominent hypothesis in the field suggests that some benefits of sleep are mediated by a broad but selective weakening, or scaling-down, of synaptic strength during sleep in order to offset increased excitability from synaptic potentiation during wake. The literature also shows that synapses can be strengthened during sleep, raising the question of what molecular mechanisms may allow for selection of synaptic plasticity types during sleep. Here I describe mechanisms of action of the scaling factors Arc and Homer1a in selective plasticity and links with sleep need. Arc and Homer1a are induced in neurons in response to waking neuronal activity and accumulate with time spent awake. I suggest that during sleep, Arc and Homer1a drive broad weakening of synapses through homeostatic scaling-down, but in a manner that is sensitive to the plasticity history of individual synapses, based on patterned phosphorylation of synaptic proteins. Therefore, Arc and Homer1a may offer insights into the intricate links between a cellular basis of sleep need and memory consolidation during sleep.
DOI: 10.7554/elife.66304
发表时间: 2021-06-21
期刊: eLife
影响因子: 7.7
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