Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex

Marion Kuhn, Elias Wolf, Jonathan G. Maier, Florian Mainberger, Bernd Feige, Hanna Schmid, Jan Bürklin, Sarah Maywald, Volker Mall, Nikolai H. Jung, Janine Reis, Kai Spiegelhalder, Stefan Klöppel, Annette Sterr, Anne Eckert, Dieter Riemann, Claus Normann, Christoph Nissen

Research output: Contribution to journalArticlepeer-review

108 Scopus citations

Abstract

Sleep is ubiquitous in animals and humans, but its function remains to be further determined. The synaptic homeostasis hypothesis of sleep-wake regulation proposes a homeostatic increase in net synaptic strength and cortical excitability along with decreased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation. Here we use electrophysiological, behavioural and molecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans after sleep and sleep deprivation. We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-evoked potential and EEG theta activity) and decreased LTP-like plasticity (paired associative stimulation induced change in motor-evoked potential and memory formation) after sleep deprivation. Changes in plasma BDNF are identified as a potential mechanism. Our study indicates that sleep recalibrates homeostatic and associative synaptic plasticity, believed to be the neural basis for adaptive behaviour, in humans.

Original languageEnglish
Article number12455
JournalNature Communications
Volume7
DOIs
StatePublished - 23 Aug 2016

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