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 and Christoph Nissen ()
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Marion Kuhn: University Medical Center Freiburg
Elias Wolf: University Medical Center Freiburg
Jonathan G. Maier: University Medical Center Freiburg
Florian Mainberger: University Medical Center Freiburg
Bernd Feige: University Medical Center Freiburg
Hanna Schmid: University Medical Center Freiburg
Jan Bürklin: University Medical Center Freiburg
Sarah Maywald: University Medical Center Freiburg
Volker Mall: Technische Universität München
Nikolai H. Jung: Technische Universität München
Janine Reis: University Medical Center Freiburg
Kai Spiegelhalder: University Medical Center Freiburg
Stefan Klöppel: University Medical Center Freiburg
Annette Sterr: University of Surrey
Anne Eckert: Neurobiology Lab for Brain Aging and Mental Health, Transfaculty Research Platform University of Basel, Psychiatric University Clinics Basel
Dieter Riemann: University Medical Center Freiburg
Claus Normann: University Medical Center Freiburg
Christoph Nissen: University Medical Center Freiburg

Nature Communications, 2016, vol. 7, issue 1, 1-9

Abstract: 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.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12455

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DOI: 10.1038/ncomms12455

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