REM Sleep Deprivation Alters Learning-Induced Cell Proliferation and Generation of Newborn Young Neurons in the Dentate Gyrus of the Dorsal Hippocampus

Author(s):  
Shweta Tripathi ◽  
Sushil K. Jha
2008 ◽  
Vol 294 (5) ◽  
pp. R1693-R1703 ◽  
Author(s):  
Anka D. Mueller ◽  
Michael S. Pollock ◽  
Stephanie E. Lieblich ◽  
Jonathan R. Epp ◽  
Liisa A. M. Galea ◽  
...  

Sleep deprivation (SD) can suppress cell proliferation in the hippocampal dentate gyrus of adult male rodents, suggesting that sleep may contribute to hippocampal functions by promoting neurogenesis. However, suppression of cell proliferation in rats by the platform-over-water SD method has been attributed to elevated corticosterone (Cort), a potent inhibitor of cell proliferation and nonspecific correlate of this procedure. We report here results that do not support this conclusion. Intact and adrenalectomized (ADX) male rats were subjected to a 96-h SD using multiple- and single-platform methods. New cells were identified by immunoreactivity for 5-bromo-2′-deoxyuridine (BrdU) or Ki67 and new neurons by immunoreactivity for BrdU and doublecortin. EEG recordings confirmed a 95% deprivation of rapid eye movement (REM) sleep and a 40% decrease of non-REM sleep. Cell proliferation in the dentate gyrus was suppressed by up to 50% in sleep-deprived rats relative to apparatus control or home cage control rats. This effect was also observed in ADX rats receiving continuous low-dose Cort replacement via subcutaneous minipumps but not in ADX rats receiving Cort replacement via drinking water. In these latter rats, Cort intake via water was reduced by 60% during SD; upregulation of cell proliferation by reduced Cort intake may obscure inhibitory effects of sleep loss on cell proliferation. SD had no effect on the percentage of new cells expressing a neuronal phenotype. These results demonstrate that the Cort replacement method is critical for detecting an effect of SD on cell proliferation and support a significant role for sleep in adult neurogenesis.


2021 ◽  
Author(s):  
Sang-Min Kim ◽  
Seungjae Zhang ◽  
Jiwon Park ◽  
Hyun Jae Sung ◽  
Thuy-Duong Thi Tran ◽  
...  

1967 ◽  
Vol 24 (3) ◽  
pp. 851-858 ◽  
Author(s):  
H. W. AGNEW ◽  
WILSE B. WEBB ◽  
ROBERT L. WILLIAMS

2019 ◽  
Vol 109 ◽  
pp. 1563-1568
Author(s):  
Mohammad Nasehi ◽  
Ameneh Shirkhodaei ◽  
Mohaddeseh Ebrahimi-Ghiri ◽  
Mohammad-Reza Zarrindast

SLEEP ◽  
2002 ◽  
Vol 25 (8) ◽  
pp. 37-41 ◽  
Author(s):  
Hiromi Ohno ◽  
Ryo Urushihara ◽  
Hiroyoshi Sei ◽  
Yusuke Morita

1995 ◽  
Vol 268 (6) ◽  
pp. R1456-R1463 ◽  
Author(s):  
T. Porkka-Heiskanen ◽  
S. E. Smith ◽  
T. Taira ◽  
J. H. Urban ◽  
J. E. Levine ◽  
...  

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.


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