期刊
NEURON
卷 75, 期 6, 页码 1105-1113出版社
CELL PRESS
DOI: 10.1016/j.neuron.2012.08.034
关键词
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资金
- Canadian Institutes of Health Research [MOP-67175, MOP-37862]
- Natural Science and Engineering Research Council of Canada [298475]
- National Institute of Neurological Disorders and Stroke [1R01NS060870, 1R01 NS059740]
- Fonds de la Recherche en Sante du Quebec via Chercheur National program
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 coactivation 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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