Cited by 177Sleep and Wakefulness ResearchNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Paradoxical (REM) Sleep Deprivation Causes a Large and Rapidly Reversible Decrease in Long-Term Potentiation, Synaptic Transmission, Glutamate Receptor Protein Levels, and ERK/MAPK Activation in the Dorsal Hippocampus

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Ravassard, Pascal, Pachoud, Bastien, Comte, Jean-Christophe, Mejia-Perez, Camila, Scoté-Blachon, Céline, Gay, Nadine, Claustrat, Bruno, Touret, Monique +2 more·2009·Sleep

Abstract

STUDY OBJECTIVES: It has been shown that wake (W) and slow wave sleep (SWS) modulate synaptic transmission in neocortical projections. However the impact of paradoxical sleep (PS) quantities on synaptic transmission remains unknown. We examined whether PS modulated the excitatory transmission and expression of glutamate receptor subtypes and phosphorylated extracellular signal-regulated kinases (p-ERK1/2). DESIGN: PS deprivation (PSD) was carried out with the multiple platforms method on adult male Sprague-Dawley rats. LTP, late-LTP, and synaptic transmission were studied in the dorsal and ventral hippocampus of controls, 75-h PSD and 150-min PS rebound (PSR). GluR1 and NR1 protein and mRNA expression were evaluated by western blot and real-time PCR. p-ERK1/2 level was quantified by western blot and immunohistochemistry. MEASUREMENT AND RESULTS: PSD decreased synaptic transmission and LTP selectively in dorsal CA1 and PSR rescued these deficits. PSD-induced synaptic modifications in CA1 were associated with a decrease in GluR1, NR1, and p-ERK1/2 levels in dorsal CA1 without change in GluR1 and NR1 mRNA expression. Regression analysis shows that LTP is positively correlated with both PS quantities and SWS episodes duration, whereas synaptic transmission and late-LTP are positively correlated with PS quantities and negatively correlated with SWS quantities. CONCLUSIONS: These findings unveil previously unrecognized roles of PSD on synaptic transmission and LTP in the dorsal, but not in the ventral, hippocampus. The fact that the decrease in protein expression of GluR1 and NR1 was not associated with a change in mRNA expression of these receptors suggests that a sleep-induced modulation of translational mechanisms occurs in dorsal CA1.

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Crossref · 10.1093/sleep/32.2.227

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  • Selective deprivation of REM sleep appears to be sufficient for producing an impairment in LTP induction.

    “Selective deprivation of REM sleep appears to be sufficient for producing an impairment in LTP induction (269,270,596,636,743,970,1010).”

    From About Sleep's Role in Memory (2013) · cites this paper as [970]

    Figure 1 reports that one tetanus failed to induce robust LTP in slices from REM-sleep-deprived rats, supporting impaired LTP induction. But the paper also states that its deprivation procedure altered slow-wave sleep and that fragmentation of both REM and slow-wave sleep may affect the threshold for LTP induction. It therefore does not establish that selective loss of REM sleep alone is sufficient. (LLM, conf=0.86)

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Research works printed but not linked: 5

  1. Yang CH, Huang CC, Hsu KS. Behavioral stress modifies hip- pocampal synaptic plasticity through corticosterone-induced sleep on the maintenance of hippocampal and medial prefrontal cortex LTP. Eur J Neurosci 2004;20:3453-62.
  2. Andersen P. Long-term potentiation-outstanding problems. In: Changeux JP, Konishi, M., ed. The neural and molecular bases of learning. Chichester: John Wiley & Sons, 1987:239-62.
  3. sustained extracellular signal-regulated kinase/mitogen-activated protein kinase activation. J Neurosci 2004;24:11029-34.
  4. Dutuit M, Didier-Bazes M, Vergnes M, et al. Specific alteration in the expression of glial fibrillary acidic protein, glutamate dehy- drogenase, and glutamine synthetase in rats with genetic absence epilepsy. Glia 2000;32:15-24.
  5. Moser MB, Moser EI. Functional differentiation in the hippocam- pus. Hippocampus 1998;8:608-19.

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Authors
Ravassard, P., Pachoud, B., Comte, J.-C., Mejia-Perez, C., Scoté-Blachon, C., Gay, N., Claustrat, B., Touret, M., Luppi, P.-H., & Salin, P. A.
Affiliations
  • Lyon 1 Université (FR)
  • Centre d'Exploration et de Recherche Médicale par Emission de Positons (FR)
  • Inserm (FR)
Corresponding author
Ravassard, Pascal
Venue
Sleep
Published
2009-02
Volume
32
Issue
2
Pages
227-240
ISSN
  • 0161-8105 (ISSN-L)
  • 1550-9109
OpenAlex
W1539823279
Cited by
177
References
56
Citations by year
2026: 2 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 13 · 2021: 4 · 2020: 12 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 6 · 2015: 19 · 2014: 18 · 2013: 18 · 2012: 8
FWCI
6.15
Type
journal article
Language
en
Open access
Locations
  • SLEEP (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
  • UCL Discovery (University College London) (submittedVersion)
Funders
Institut National de la Santé et de la Recherche Médicale
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
REM sleep deprivation, REM sleep, long-term potentiation, synaptic transmission, dorsal hippocampus, CA1, glutamate receptor subunits, GluR1, NR1, ERK signaling, slow-wave sleep, sleep rebound, translational regulation, synaptic plasticity
MeSH terms
Animals, Enzyme Activation, Hippocampus, Male, Synaptic Transmission, RNA, Messenger, Sleep Deprivation, Sleep, REM, Protein Biosynthesis, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Long-Term Potentiation, Receptors, AMPA, Mitogen-Activated Protein Kinase 1, Reverse Transcriptase Polymerase Chain Reaction, Mitogen-Activated Protein Kinase 3, Rats

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