Paradoxical sleep: A vigilance state to gate long-term brain plasticity?

Pascal Ravassard, Al Mahdy Hamieh, Gaël Malleret, Paul-Antoine Salin
Neurobiology of Learning and Memory. 2015-07-01; 122: 4-10
DOI: 10.1016/j.nlm.2014.11.013

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1. Neurobiol Learn Mem. 2015 Jul;122:4-10. doi: 10.1016/j.nlm.2014.11.013. Epub 2014
Nov 28.

Paradoxical sleep: A vigilance state to gate long-term brain plasticity?

Ravassard P(1), Hamieh AM(1), Malleret G(1), Salin PA(2).

Author information:
(1)Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche
5292, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité
1028, France; Physiopathology of the Sleep Neuronal Networks, Lyon Neuroscience
Research Center, F-69008 Lyon, France; University Lyon 1, F-69000 Lyon, France.
(2)Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche
5292, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité
1028, France; Physiopathology of the Sleep Neuronal Networks, Lyon Neuroscience
Research Center, F-69008 Lyon, France; University Lyon 1, F-69000 Lyon, France.
Electronic address: .

Memory consolidation is the process for long-term storage of information and
protection against interferences. It has been proposed that long-term
potentiation (LTP), the long-lasting enhancement of synaptic transmission, is a
cellular model for memory consolidation. Since consolidation of several forms of
memory is facilitated by paradoxical sleep (PS) we ask whether PS modulates the
cellular and molecular pathways underlying LTP. The long-lasting form of LTP
(L-LTP) is dependent on the activation of transcription factors, enzymatic
cascades and the secreted neurotrophin BDNF. By using PS deprivation,
immunohistochemistry and quantitative real-time polymerase chain reaction (qPCR),
we showed that an increase in PS amount (produced by rebound in PS deprived rats)
is able to up-regulate the expression level of transcription factors Zif268 and
c-Fos as well as Arc and BDNF in the CA1 and CA3 areas of the hippocampus.
Several studies involved these factors in dendritic protein synthesis and in
long-term structural changes of synapses underlying L-LTP. The present study
together with the work of others (Ribeiro et al., 2002) suggest that by this
mechanism, a post-learning increase in PS quantity (post-learning PS window)
could convert a transient form of LTP to L-LTP.

Copyright © 2014 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.nlm.2014.11.013
PMID: 25448317 [Indexed for MEDLINE]

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