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.
OBJECTIVE
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).


METHODS
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.


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.
Ravassard
Pascal
P
UMR 5167 CNRS, Physio-pathologie des reseaux neuronaux du cycle veille-sommeil, Institut Feddratifdes Neurosciences de Lyon (IFNL, IFR 19), Université Lyon, Lyon, France.
Pachoud
Bastien
B
Comte
Jean-Christophe
JC
Mejia-Perez
Camila
C
Scoté-Blachon
Celine
C
Gay
Nadine
N
Claustrat
Bruno
B
Touret
Monique
M
Luppi
Pierre-Hervé
PH
Salin
Paul Antoine
PA
D000818:Animals; D004789:Enzyme Activation / Q000235:genetics; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology; D017774:Long-Term Potentiation / Q000235:genetics* / Q000502:physiology; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics; D014176:Protein Biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000235:genetics*; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012892:Sleep Deprivation / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D012895:Sleep, REM / Q000235:genetics / Q000502:physiology; D009435:Synaptic Transmission / Q000235:genetics* / Q000502:physiology
D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D012333:RNA, Messenger; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; C409466:NR1 NMDA receptor; C535149:Mapk1 protein, rat