Department of Psychiatry, University of Wisconsin, Madison, WI 53719, USA.
Science. 2011 Jun 24;332(6037):1576-81. doi: 10.1126/science.1202839.
The functions of sleep remain elusive, but a strong link exists between sleep need and neuronal plasticity. We tested the hypothesis that plastic processes during wake lead to a net increase in synaptic strength and sleep is necessary for synaptic renormalization. We found that, in three Drosophila neuronal circuits, synapse size or number increases after a few hours of wake and decreases only if flies are allowed to sleep. A richer wake experience resulted in both larger synaptic growth and greater sleep need. Finally, we demonstrate that the gene Fmr1 (fragile X mental retardation 1) plays an important role in sleep-dependent synaptic renormalization.
睡眠的功能仍然难以捉摸，但睡眠需求和神经元可塑性之间存在很强的联系。我们检验了这样一个假设，即在清醒时的可塑性过程会导致突触强度的净增加，而睡眠对于突触的正常化是必要的。我们发现，在三个果蝇神经元回路中，突触大小或数量在几个小时的清醒后增加，只有在允许果蝇睡眠时才会减少。更丰富的清醒体验会导致更大的突触生长和更大的睡眠需求。最后，我们证明了基因 Fmr1（脆性 X 智力低下 1）在睡眠依赖性突触正常化中起着重要作用。
