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矛盾的树突-胞体解耦支持快速眼动睡眠期间的皮质可塑性。

Paradoxical somatodendritic decoupling supports cortical plasticity during REM sleep.

作者信息

Aime Mattia, Calcini Niccolò, Borsa Micaela, Campelo Tiago, Rusterholz Thomas, Sattin Andrea, Fellin Tommaso, Adamantidis Antoine

机构信息

Zentrum für Experimentelle Neurologie, Department of Neurology, Inselspital University Hospital Bern, Bern, Switzerland.

Department of Biomedical Research, University of Bern, Bern, Switzerland.

出版信息

Science. 2022 May 13;376(6594):724-730. doi: 10.1126/science.abk2734. Epub 2022 May 12.

DOI:10.1126/science.abk2734
PMID:35549430
Abstract

Rapid eye movement (REM) sleep is associated with the consolidation of emotional memories. Yet, the underlying neocortical circuits and synaptic mechanisms remain unclear. We found that REM sleep is associated with a somatodendritic decoupling in pyramidal neurons of the prefrontal cortex. This decoupling reflects a shift of inhibitory balance between parvalbumin neuron-mediated somatic inhibition and vasoactive intestinal peptide-mediated dendritic disinhibition, mostly driven by neurons from the central medial thalamus. REM-specific optogenetic suppression of dendritic activity led to a loss of danger-versus-safety discrimination during associative learning and a lack of synaptic plasticity, whereas optogenetic release of somatic inhibition resulted in enhanced discrimination and synaptic potentiation. Somatodendritic decoupling during REM sleep promotes opposite synaptic plasticity mechanisms that optimize emotional responses to future behavioral stressors.

摘要

快速眼动(REM)睡眠与情绪记忆的巩固有关。然而,其潜在的新皮质回路和突触机制仍不清楚。我们发现,REM睡眠与前额叶皮质锥体细胞的体树突解耦有关。这种解耦反映了小白蛋白神经元介导的体细胞抑制和血管活性肠肽介导的树突去抑制之间抑制平衡的转变,这主要由丘脑中央内侧核的神经元驱动。REM特异性光遗传学抑制树突活动导致联想学习过程中危险与安全辨别能力的丧失以及突触可塑性的缺乏,而体细胞抑制的光遗传学释放则导致辨别能力增强和突触增强。REM睡眠期间的体树突解耦促进了相反的突触可塑性机制,这些机制优化了对未来行为应激源的情绪反应。

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