Chronic sleep restriction impairs spatial memory in rats

McCoy, John G.; Christie, Michael A.; Kim, Youngsoo; Brennan, Robert W.; Poeta, Devon L.; McCarley, Robert W.; Strecker, Robert E.

doi:10.1097/wnr.0b013e32835cd97a

Cited by 26 publications

(26 citation statements)

References 24 publications

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“…When analysing the effect of sleep disorders on memory parameters, Guan et al (8) and McCoy et al (35) showed that, compared with the control group, those in the sleep-deprived group had decreased time in the target quadrant. Aricanli (36) found that rats that were deprived of REM sleep for 13 days spent less time in the target quadrant, compared with those in the control group, but the results were not statistically signifi cant.…”

Section: Discussionmentioning

confidence: 99%

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Saygın¹,

Özgüner²,

Önder³

et al. 2017

BLL

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BACKGROUND: To examine the impact of different types of sleep deprivation on hippocampal-mediated learning and memory in rats. METHODS: Forty-eight Sprague-Dawley male rats were randomly assigned to 1 of 4 equal-size groups: (1) 12 hours of sleep per day (control). (2) total sleep deprivation (TSD), (3) rapid eye movement (REM) deprivation (RD), and (4) sleep restricted to 4 hours per day (SR). All rats were subjected to swimming training in the Morris water maze (MWM). At the end of the experiments, the rats were decapitated, and hippocampus tissue was analyzed for several neurotransmitters and receptors. RESULTS: The time spent at the target quadrant increased from 20.2 to 30.0 seconds in the control group on the third day of the experiment, whereas corresponding values increased from 20.2 to 21.8 seconds in the TSD group, 22.1 to 25.4 seconds in the RD group, and 21.2 to 32.0 sec in the SR group (p = 0.026). On the seventh day of the experiment, the values decreased to 25.0 seconds in controls, 22.5 in the RD group, and 23.6 in the SR group (p = 0.045). The TSD group demonstrated signifi cant decreases in glutamate and serotonin levels compared with the control group. There was a signifi cant increase in 5-HT2 a receptor expression in all intervention groups compared with the controls. CONCLUSIONS: Our results of glutamate levels and 5-HT2a receptor expression in the hippocampus seem to be primarily involved in sleep and memory regulation (Tab. 2, Fig. 4, Ref. 59). Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 99%

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Saygın¹,

Özgüner²,

Önder³

et al. 2017

BLL

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“…We also found that brain BDNF expression was reduced within the hippocampus after CSR and not enhanced in the cortex after multiple days of SR. Overall, the current findings indicate elevated brain pro-inflammatory cytokines and attenuated hippocampal BDNF expression are induced by CSR, which could potentially contribute to CSR-related impairments in cognition and alterations in SWA [2,7]. …”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicates that chronic sleep restriction (CSR), a condition prevalent in today's societies, impairs health, immune functioning [1], and cognition [2,3]. These functions are regulated by inflammatory and synaptic plasticity-related molecules [4].…”

Section: Introductionmentioning

confidence: 99%

Chronic sleep restriction elevates brain interleukin-1 beta and tumor necrosis factor-alpha and attenuates brain-derived neurotrophic factor expression

Zielinski

Kim

Karpova

et al. 2014

Neuroscience Letters

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118

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Acute sleep loss increases pro-inflammatory and synaptic plasticity-related molecules in the brain, including interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and brain-derived neurotrophic factor (BDNF). These molecules enhance non-rapid eye movement sleep slow wave activity (SWA), also known as electroencephalogram delta power, and modulate neurocognitive performance. Evidence suggests that chronic sleep restriction (CSR), a condition prevalent in today's society, does not elicit the enhanced SWA that is seen after acute sleep loss, although it cumulatively impairs neurocognitive functioning. Rats were continuously sleep deprived for 18 h per day and allowed 6 h of ad libitum sleep opportunity for 1 (SR1), 3 (SR3), or 5 (SR5) successive days (i.e., CSR). IL-1β, TNF-α, and BDNF mRNA levels were determined in the somatosensory cortex, frontal cortex, hippocampus, and basal forebrain. Largely, brain IL-1β and TNF-α expression were significantly enhanced throughout CSR. In contrast, BDNF mRNA levels were similar to baseline values in the cortex after 1 day of SR and significantly lower than baseline values in the hippocampus after 5 days of SR. In the basal forebrain, BDNF expression remained elevated throughout the 5 days of CSR, although IL-1β expression was significantly reduced. The chronic elevations of IL-1β and TNF-α and inhibition of BDNF might contribute to the reported lack of SWA responses reported after CSR. Further, the CSR-induced enhancements in brain inflammatory molecules and attenuations in hippocampal BDNF might contribute to neurocognitive and vigilance detriments that occur from CSR.

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“…Sleep deprivation has been shown to impair memory consolidation in numerous human and rodent studies (3), including rat and mouse CSR paradigms (48,49), suggesting that compensatory processes which may be initiated are certainly insufficient. We suggest however, that the results of the current study may open a window on the organization of cortical networks to serve diverse sleep functions.…”

Section: The Pattern Of Rem Sleep Rebound Is Mirrored In Eeg Slowmentioning

confidence: 99%

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

Kim

Kocsis

Hwang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Homeostatic rebound in rapid eye movement (REM) sleep normally occurs after acute sleep deprivation, but REM sleep rebound settles on a persistently elevated level despite continued accumulation of REM sleep debt during chronic sleep restriction (CSR). Using highdensity EEG in mice, we studied how this pattern of global regulation is implemented in cortical regions with different functions and network architectures. We found that across all areas, slow oscillations repeated the behavioral pattern of persistent enhancement during CSR, whereas high-frequency oscillations showed progressive increases. This pattern followed a common rule despite marked topographic differences. The findings suggest that REM sleep slow oscillations may translate top-down homeostatic control to widely separated brain regions whereas fast oscillations synchronizing local neuronal ensembles escape this global command. These patterns of EEG oscillation changes are interpreted to reconcile two prevailing theories of the function of sleep, synaptic homeostasis and sleep dependent memory consolidation. There has been substantial recent progress in understanding the neuronal mechanisms of two seemingly unrelated but, more likely, complementary functions of sleep. The first, conceptualized as the synaptic homeostasis theory (1), produced experimental evidence for a global downscaling of synaptic strength during sleep to offset the unsustainable upscaling associated with neuronal activation during the preceding period of wakefulness (2). The second line of research keeps accumulating data to support an active role of sleep in offline memory processing (3) and argues that certain synapses not only escape global downscaling in sleep but instead are potentiated; firing rate and synchrony in select neuronal ensembles representing newly acquired and deemed relevant information are increased. The mechanisms of how these two proposed functions of sleep are reconciled on the network or ensemble level are poorly understood.From the very beginning, both processes were linked to specific oscillatory patterns of neuronal activity. The synaptic homeostasis hypothesis, and sleep homeostatic regulation in general, was correlated with EEG delta power (4) and memory consolidation was associated with episodic fast oscillations during non-REM (NREM) sleep (5). Recent evidence from network level investigations concur. On the one hand, different measures of homeostatic downscaling on the neuronal level (synaptic depotentiation, decrease in firing rate, decreased synchrony, etc.) were shown to correlate with the global decrease in delta power (6). On the other hand, reactivation of memory traces primarily occur during spindle-ripple events (7) and requires the temporal organization provided by local fast oscillations for coordination of firing within local neuronal ensembles.Slow and fast oscillations, respectively, support global and local processing, not only in NREM sleep but also in any brain state, in general. Slow oscillations (delta, theta, alpha, beta1) all...

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Chronic sleep restriction impairs spatial memory in rats

Cited by 26 publications

References 24 publications

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Chronic sleep restriction elevates brain interleukin-1 beta and tumor necrosis factor-alpha and attenuates brain-derived neurotrophic factor expression

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

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