Sleep oscillations in the thalamocortical system induce long-term neuronal plasticity.

Sleep oscillations in the thalamocortical system induce long-term neuronal plasticity.
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DOI:
10.1016/j.neuron.2012.08.034
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发表时间:
2012-09-20
期刊:
影响因子:
16.2
通讯作者:
Timofeev I
Timofeev I
中科院分区:
医学1区
文献类型:
--
作者:
Chauvette S;Seigneur J;Timofeev I

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长期可塑性有助于记忆形成,而睡眠在记忆巩固中起着至关重要的作用。然而,尚不清楚睡眠慢振荡本身是否会引起有助于记忆保留的长期可塑性。使用 1 Hz 的体内丘脑前电刺激(其本身不会引起诱发反应的立即增强),我们研究了不同警觉状态如何调节皮质诱发反应。我们发现,与之前的清醒发作相比,慢波睡眠发作(睡眠期间有或没有刺激)后觉醒期间的体感诱发电位增强。在体外,我们确定这种增强具有钙依赖性的突触后机制,需要超极化周期(慢波),并且需要 AMPA 和 NMDA 受体的共同激活。我们的研究结果表明,长时程增强发生在慢波睡眠期间,支持其对记忆的贡献。
Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo pre-thalamic electrical stimulation at 1 Hz which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium-dependent, requires hyperpolarization periods (slow waves), and requires a co-activation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep supporting its contribution to memory.
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影响因子: 34.7
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