Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex.
Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex.
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DOI：
10.1038/ncomms12455
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发表时间：
2016-08-23
影响因子：
16.6
通讯作者：
Nissen C
中科院分区：
文献类型：
--
作者：
Kuhn M;Wolf E;Maier JG;Mainberger F;Feige B;Schmid H;Bürklin J;Maywald S;Mall V;Jung NH;Reis J;Spiegelhalder K;Klöppel S;Sterr A;Eckert A;Riemann D;Normann C;Nissen C
睡眠在动物和人类中普遍存在，但其功能仍有待进一步确定。睡眠-觉醒调节的突触内稳态假说认为，睡眠剥夺后，由于饱和，突触净强度和皮层兴奋性沿着增加，同时联合突触长时程增强（LTP）的诱导减少。在这里，我们使用电生理，行为和分子指标，非侵入性地研究睡眠和睡眠剥夺后人类的净突触强度和LTP样可塑性。我们证明了睡眠剥夺后净突触强度增加（TMS强度引起运动诱发电位和EEG θ活动的预定义幅度）和LTP样可塑性降低（配对联想刺激诱导运动诱发电位和记忆形成的变化）的指数。血浆BDNF的变化被确定为一个潜在的机制。我们的研究表明，睡眠可以重新校准稳态和关联突触可塑性，这被认为是人类适应行为的神经基础。 主要基于动物研究的发现，睡眠剥夺被认为导致突触强度的稳态增加和相关LTP的诱导减少。在此，Kuhn等人证明了人类沿着血浆BDNF水平改变的类似睡眠依赖性突触可塑性变化。
Sleep is ubiquitous in animals and humans, but its function remains to be further determined. The synaptic homeostasis hypothesis of sleep–wake regulation proposes a homeostatic increase in net synaptic strength and cortical excitability along with decreased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation. Here we use electrophysiological, behavioural and molecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans after sleep and sleep deprivation. We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-evoked potential and EEG theta activity) and decreased LTP-like plasticity (paired associative stimulation induced change in motor-evoked potential and memory formation) after sleep deprivation. Changes in plasma BDNF are identified as a potential mechanism. Our study indicates that sleep recalibrates homeostatic and associative synaptic plasticity, believed to be the neural basis for adaptive behaviour, in humans. Sleep deprivation is believed to lead to homeostatic increases in synaptic strength and reduced inducibility of associative LTP, based mainly on findings from animal studies. Here, Kuhn et al. demonstrate similar sleep-dependent synaptic plasticity changes in humans along with altered plasma BDNF levels.