Ultrastructural evidence for synaptic scaling across the wake/sleep cycle
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- Luisa de Vivo
- Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
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- Michele Bellesi
- Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
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- William Marshall
- Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
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- Eric A. Bushong
- National Center for Microscopy and Imaging Research, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
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- Mark H. Ellisman
- National Center for Microscopy and Imaging Research, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
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- Giulio Tononi
- Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
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- Chiara Cirelli
- Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
Description
<jats:title>Synapse remodeling during sleep</jats:title> <jats:p> General activity and information processing while an animal is awake drive synapse strengthening. This is counterbalanced by weakening of synapses during sleep (see the Perspective by Acsády). De Vivo <jats:italic>et al.</jats:italic> used serial scanning electron microscopy to reconstruct axon-spine interface and spine head volume in the mouse brain. They observed a substantial decrease in interface size after sleep. The largest relative changes occurred among weak synapses, whereas strong ones remained stable. Diering <jats:italic>et al.</jats:italic> found that synapses undergo changes in synaptic glutamate receptors during the sleep-wake cycle, driven by the immediate early gene <jats:italic>Homer1a.</jats:italic> In awake animals, <jats:italic>Homer1a</jats:italic> accumulates in neurons but is excluded from synapses by high levels of noradrenaline. At the onset of sleep, noradrenaline levels decline, allowing <jats:italic>Homer1a</jats:italic> to move to excitatory synapses and drive synapse weakening. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6324" page="457" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aam7917">457</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6324" page="507" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah5982">507</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6324" page="511" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aai8355">511</jats:related-article> </jats:p>
Journal
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- Science
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Science 355 (6324), 507-510, 2017-02-03
American Association for the Advancement of Science (AAAS)
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Details 詳細情報について
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- CRID
- 1361699993681692672
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- ISSN
- 10959203
- 00368075
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- Data Source
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- Crossref