Sleep Oscillations in the Thalamocortical System Induce Long-Term Neuronal Plasticity

• Published in: Neuron (Cambridge, Mass.) Vol. 75; no. 6; pp. 1105 - 1113
• Main Authors: Chauvette, Sylvain, Seigneur, Josée, Timofeev, Igor
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 20.09.2012; Elsevier Limited
• Subjects: 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology; Analysis of Variance; Animals; Animals, Newborn; Cats; Chelating Agents - pharmacology; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Electric Stimulation; Electromyography; Electrooculography; Evoked Potentials - physiology; Excitatory Amino Acid Antagonists - pharmacology; Experiments; In Vitro Techniques; Medical research; Neuronal Plasticity - physiology; Neurons - physiology; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Signal processing; Sleep - physiology; Software; Somatosensory Cortex - cytology; Somatosensory Cortex - physiology; Statistics, Nonparametric; Thalamus - physiology; Valine - analogs & derivatives; Valine - pharmacology; Wakefulness - physiology
• ISSN: 0896-6273; 1097-4199; 1097-4199
• DOI: 10.1016/j.neuron.2012.08.034

Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo prethalamic electrical stimulation at 1 Hz, which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium dependent, requires hyperpolarization periods (slow waves), and requires a coactivation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep, supporting its contribution to memory. ► Slow-wave sleep induces long-term potentiation of evoked responses ► In vitro, stimulation mimicking SWS replicated these results ► Potentiation of responses was postsynaptic, Ca2+, AMPA, and NMDA dependent ► The mechanism of potentiation was compatible with the classical LTP mechanism Sleep contributes to memory formation, but the physiological basis of this contribution is not clear. Chauvette et al. show that cortical evoked responses are increased after slow-wave sleep and this increase is compatible with the classical long-term potentiation.