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The Journal of Neuroscience, July 15, 2009, 29(28):9026-9041; doi:10.1523/JNEUROSCI.1215-09.2009

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Behavioral/Systems/Cognitive
NR2A at CA1 Synapses Is Obligatory for the Susceptibility of Hippocampal Plasticity to Sleep Loss

Fabio Longordo,¹ Caroline Kopp,² Masayoshi Mishina,³ Rafael Luján,⁴ and Anita Lüthi¹

¹Department of Cell Biology and Morphology, University of Lausanne, CH-1005 Lausanne, Switzerland, ²Biozentrum, University of Basel, CH-4009 Basel, Switzerland, ³Department of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, The University of Tokyo, 113-0033 Tokyo, Japan, and ⁴Departamento de Ciencias Medicas, Facultad de Medicina, Universidad de Castilla-La Mancha, 02006 Albacete, Spain

Correspondence should be addressed to Anita Lüthi, Department of Cell Biology and Morphology, University of Lausanne, Rue du Bugnon 9, CH-1005 Lausanne, Switzerland. Email: anita.luthi{at}unil.ch

A loss in the necessary amount of sleep alters expression of genes and proteins implicated in brain plasticity, but key proteins that render neuronal circuits sensitive to sleep disturbance are unknown. We show that mild (4–6 h) sleep deprivation (SD) selectively augmented the number of NR2A subunits of NMDA receptors on postsynaptic densities of adult mouse CA1 synapses. The greater synaptic NR2A content facilitated induction of CA3-CA1 long-term depression in the theta frequency stimulation range and augmented the synaptic modification threshold. NR2A-knock-out mice maintained behavioral response to SD, including compensatory increase in post-deprivation resting time, but hippocampal synaptic plasticity was insensitive to sleep loss. After SD, the balance between synaptically activated and slowly recruited NMDA receptor pools during temporal summation was disrupted. Together, these results indicate that NR2A is obligatory for the consequences of sleep loss on hippocampal synaptic plasticity. These findings could advance pharmacological strategies aiming to sustain hippocampal function during sleep restriction.

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Received March 11, 2009; revised May 26, 2009; accepted June 11, 2009.

Correspondence should be addressed to Anita Lüthi, Department of Cell Biology and Morphology, University of Lausanne, Rue du Bugnon 9, CH-1005 Lausanne, Switzerland. Email: anita.luthi{at}unil.ch

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