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首页> 外文期刊>Neuron >Mechanisms of sleep-dependent consolidation of cortical plasticity.
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Mechanisms of sleep-dependent consolidation of cortical plasticity.

机译：睡眠依赖的皮质可塑性巩固机制。

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Sleep is thought to consolidate changes in synaptic strength, but the underlying mechanisms are unknown. We investigated the cellular events involved in this process during ocular dominance plasticity (ODP)-a canonical form of in vivo cortical plasticity triggered by monocular deprivation (MD) and consolidated by sleep via undetermined, activity-dependent mechanisms. We find that sleep consolidates ODP primarily by strengthening cortical responses to nondeprived eye stimulation. Consolidation is inhibited by reversible, intracortical antagonism of NMDA receptors (NMDARs) or cAMP-dependent protein kinase (PKA) during post-MD sleep. Consolidation is also associated with sleep-dependent increases in the activity of remodeling neurons and in the phosphorylation of proteins required for potentiation of glutamatergic synapses. These findings demonstrate that synaptic strengthening via NMDAR and PKA activity is a key step in sleep-dependent consolidation of ODP.
机译：人们认为睡眠可以巩固突触强度的变化，但其潜在机制尚不清楚。我们调查了眼优势可塑性（ODP）-单眼剥夺（MD）触发的体内皮质可塑性的典型形式，并通过不确定的活动依赖机制通过睡眠巩固了这一过程中的细胞事件。我们发现睡眠主要通过增强皮质对非剥夺性眼刺激的反应来巩固ODP。 MD睡眠后，NMDA受体（NMDARs）或cAMP依赖性蛋白激酶（PKA）可逆的皮质内拮抗作用抑制了固结。巩固还与重塑神经元的活性和增强谷氨酸能突触所需的蛋白质的磷酸化有关的睡眠依赖性增加有关。这些发现表明通过NMDAR和PKA活性的突触加强是ODP的睡眠依赖性巩固中的关键步骤。

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