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

•Paradoxical sleep (PS) facilitates consolidation of hippocampal based forms of memory•Long term potentiation (LTP) in the hippocampus is required for memory consolidation•PS increases the expression of Zif268, c-Fos, BDNF and Arc in the hippocampus•Zif268, c-Fos, BDNF and Arc are required in hippoc...

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Bibliographic Details
Published in:Neurobiology of learning and memory 2015-07, Vol.122, p.4-10
Main Authors: Ravassard, Pascal, Hamieh, Al Mahdy, Malleret, Gaël, Salin, Paul-Antoine
Format: Article
Language:English
Subjects:
Animals
Arousal
BDNF
Brain research
c-Fos
Early Growth Response Protein 1 - metabolism
Hippocampus - metabolism
Hippocampus - physiology
Immunohistochemistry
Learning
Long-Term Potentiation
LTP and L-LTP
Male
Memory
Memory Consolidation - physiology
Post-learning paradoxical sleep window
Rats, Sprague-Dawley
Sleep
Sleep, REM - physiology
Zif268 also known as EGR-1
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Summary:•Paradoxical sleep (PS) facilitates consolidation of hippocampal based forms of memory•Long term potentiation (LTP) in the hippocampus is required for memory consolidation•PS increases the expression of Zif268, c-Fos, BDNF and Arc in the hippocampus•Zif268, c-Fos, BDNF and Arc are required in hippocampal LTP•This result suggests molecular mechanisms by which PS enhances memory consolidation 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 enhancementof 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.
ISSN:1074-7427
1095-9564
DOI:10.1016/j.nlm.2014.11.013