scholarly journals Daily Acclimation Handling Does Not Affect Hippocampal Long-Term Potentiation or Cause Chronic Sleep Deprivation in Mice

SLEEP ◽  
2013 ◽  
Vol 36 (4) ◽  
pp. 601-607 ◽  
Author(s):  
Christopher G. Vecsey ◽  
Mathieu E. J. Wimmer ◽  
Robbert Havekes ◽  
Alan J. Park ◽  
Isaac J. Perron ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

The effects of long-term sleep deprivation on the long-term potentiation in the dentate gyrus and brain oxidation status in rats

2011 ◽  
Vol 70 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Cem Süer ◽  
Nazan Dolu ◽  
A. Seda Artis ◽  
Leyla Sahin ◽  
Alpaslan Yilmaz ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Oxidation Status

Sleep Deprivation Impairs Long-Term Potentiation in Rat Hippocampal Slices

2002 ◽  
Vol 88 (2) ◽  
pp. 1073-1076 ◽  
Author(s):  
I. G. Campbell ◽  
M. J. Guinan ◽  
J. M. Horowitz
Keyword(s):  
Sleep Deprivation ◽  
Neural Plasticity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Adult Rats ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Population Spike Amplitude ◽  
Specific Factors

To determine if 12-h sleep deprivation disrupts neural plasticity, we compared long-term potentiation (LTP) in five sleep-deprived and five control rats. Thirty minutes after tetanus population spike amplitude increased 101 ± 15% in 16 slices from sleep deprived rats and 139 ± 14% in 14 slices from control rats. This significant ( P < 0.05) reduction of LTP, the first demonstration that the sleep deprivation protocol impairs plasticity in adult rats, may be due to several factors. Reduced LTP may indicate that sleep provides a period of recuperation for cellular processes underlying neural plasticity. Alternatively, the stress of sleep deprivation, as indicated by elevated blood corticosterone levels, or other non-sleep-specific factors of deprivation may contribute to the LTP reduction.

scholarly journals Chronic sleep deprivation differentially affects short and long-term operant memory in Aplysia

2016 ◽  
Vol 134 ◽  
pp. 349-359 ◽  
Author(s):  
Harini C. Krishnan ◽  
Eric J. Noakes ◽  
Lisa C. Lyons
Keyword(s):  
Sleep Deprivation ◽  
Short And Long Term ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

REM sleep deprivation-induced deficits in the latency-to-peak induction and maintenance of long-term potentiation within the CA1 region of the hippocampus

2003 ◽  
Vol 973 (2) ◽  
pp. 293-297 ◽  
Author(s):  
Christopher J. Davis ◽  
Joseph W. Harding ◽  
John W. Wright
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Long Term Potentiation ◽  
Rem Sleep Deprivation ◽  
Ca1 Region ◽  
Term Potentiation

136 EFFECTS OF ETHANOL ADMINISTRATION ON LONG-TERM MEMORY DEFICIT INDUCED BY PARTIAL CHRONIC SLEEP DEPRIVATION IN MICE

2009 ◽  
Vol 10 ◽  
pp. S37
Author(s):  
L. Sanday ◽  
C.L. Patti ◽  
S.R. Kameda ◽  
M.L. Andersen ◽  
S. Tufik ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Memory Deficit ◽  
Ethanol Administration ◽  
Long Term Memory ◽  
Term Memory ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

scholarly journals Growth hormone rescues hippocampal synaptic function after sleep deprivation

2010 ◽  
Vol 298 (6) ◽  
pp. R1588-R1596 ◽  
Author(s):  
Eunyoung Kim ◽  
Lawrence M. Grover ◽  
Don Bertolotti ◽  
Todd L. Green
Keyword(s):  
Growth Hormone ◽  
Nmda Receptor ◽  
Sleep Deprivation ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Synaptic Membranes ◽  
Hippocampal Function ◽  
Synaptic Currents ◽  
Term Potentiation

Sleep is required for, and sleep loss impairs, normal hippocampal synaptic N-methyl-d-aspartate (NMDA) glutamate receptor function and expression, hippocampal NMDA receptor-dependent synaptic plasticity, and hippocampal-dependent memory function. Although sleep is essential, the signals linking sleep to hippocampal function are not known. One potential signal is growth hormone. Growth hormone is released during sleep, and its release is suppressed during sleep deprivation. If growth hormone links sleep to hippocampal function, then restoration of growth hormone during sleep deprivation should prevent adverse consequences of sleep loss. To test this hypothesis, we examined rat hippocampus for spontaneous excitatory synaptic currents in CA1 pyramidal neurons, long-term potentiation in area CA1, and NMDA receptor subunit proteins in synaptic membranes. Three days of sleep deprivation caused a significant reduction in NMDA receptor-mediated synaptic currents compared with control treatments. When rats were injected with growth hormone once per day during sleep deprivation, the loss of NMDA receptor-mediated synaptic currents was prevented. Growth hormone injections also prevented the impairment of long-term potentiation that normally follows sleep deprivation. In addition, sleep deprivation led to a selective loss of NMDA receptor 2B (NR2B) from hippocampal synaptic membranes, but normal NR2B expression was restored by growth hormone injection. Our results identify growth hormone as a critical mediator linking sleep to normal synaptic function of the hippocampus.

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