Ultrastructural evidence for synaptic scaling across the wake/sleep cycle

  • Luisa de Vivo
    Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
  • Michele Bellesi
    Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
  • William Marshall
    Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
  • Eric A. Bushong
    National Center for Microscopy and Imaging Research, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
  • Mark H. Ellisman
    National Center for Microscopy and Imaging Research, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
  • Giulio Tononi
    Department of Psychiatry, University of Wisconsin–Madison, 6001 Research Park Boulevard, Madison, WI 53719, USA.
  • 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

  • Science

    Science 355 (6324), 507-510, 2017-02-03

    American Association for the Advancement of Science (AAAS)

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