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Sleep oscillations in the thalamocortical system induce long-term neuronal plasticity.

Publication Type:

Journal Article

Source:

Neuron, Volume 75, Issue 6, p.1105-13 (2012)

Keywords:

6-Cyano-7-nitroquinoxaline-2,3-dione, Analysis of Variance, Animals, Animals, Newborn, Cats, Chelating Agents, Egtazic Acid, Electric Stimulation, Electromyography, Electrooculography, Evoked Potentials, Excitatory Amino Acid Antagonists, In Vitro Techniques, Neuronal Plasticity, Neurons, Patch-Clamp Techniques, Rats, Rats, Sprague-Dawley, Sleep, Somatosensory Cortex, Statistics, Nonparametric, Thalamus, Valine, Wakefulness

Abstract:

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.

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