Homer1a drives homeostatic scaling-down of excitatory synapses during sleep

Author:

Diering Graham H.1,Nirujogi Raja S.2,Roth Richard H.1,Worley Paul F.1,Pandey Akhilesh2,Huganir Richard L.1

Affiliation:

1. Solomon Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD, USA.

2. Department of Biological Chemistry, Institute of Genetic Medicine, Johns Hopkins University, Baltimore, MD, USA.

Abstract

Synapse remodeling during sleep 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 et al. 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 et al. found that synapses undergo changes in synaptic glutamate receptors during the sleep-wake cycle, driven by the immediate early gene Homer1a. In awake animals, Homer1a accumulates in neurons but is excluded from synapses by high levels of noradrenaline. At the onset of sleep, noradrenaline levels decline, allowing Homer1a to move to excitatory synapses and drive synapse weakening. Science , this issue p. 457 , p. 507 ; see also p. 511

Funder

NIH

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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