The Centre de Recherche Institut Universitaire en Santé Mentale de Québec-CRIUSMQ, Laval University, Québec, QC G1J 2G3, Canada.
Neuron. 2012 Sep 20;75(6):1105-13. doi: 10.1016/j.neuron.2012.08.034.
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 prethalamic 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 coactivation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep, supporting its contribution to memory.
长期可塑性有助于记忆形成，而睡眠在记忆巩固中起着关键作用。然而，睡眠慢波本身是否能诱导有助于记忆保留的长期可塑性尚不清楚。我们使用 1Hz 的丘脑前电刺激，它本身不会引起即时的诱发反应增强，来研究警觉状态的不同如何调节皮层诱发反应。我们发现，与前一个觉醒期相比，在睡眠慢波期（睡眠期间有或没有刺激）期间，体感诱发电位在觉醒时增强。在体外，我们确定这种增强具有一个依赖于钙的突触后机制，需要超极化期（慢波），并且需要 AMPA 和 NMDA 受体的共同激活。我们的结果表明，长时程增强发生在慢波睡眠期间，支持其对记忆的贡献。
