Disruptive effects of rapid eye movement sleep deprivation on long-term memory

Fishbein, William

doi:10.1016/0031-9384(71)90155-7

Cited by 130 publications

(71 citation statements)

References 20 publications

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“…These results agree with previous animal studies using various sleep-deprivation protocols and learning test paradigms that have consistently shown that post-training REM sleep deprivation can partially or even totally block improved performance (Fishbein, 1971;Pearlman, 1973;Pearlman and Becker, 1973;Shiromani and Fishbein, 1979;Smith and Butler, 1982;Smith et al, 1998). In addition to mechanical deprivation methods, another study has shown that during the post-training REM sleep window, intraperitoneal injection of the general protein synthesis inhibitor anisomycin and the cholinergic antagonist scopolamine induces marked learningmemory impairment in the rat .…”

Section: Effects Of Rem Sleep Deprivation On Learning Performancesupporting

confidence: 90%

Activation of Phasic Pontine-Wave Generator Prevents Rapid Eye Movement Sleep Deprivation-Induced Learning Impairment in the Rat: A Mechanism for Sleep-Dependent Plasticity

Datta¹,

Mavanji²,

Ulloor³

et al. 2004

J. Neurosci.

150

167

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Animal and human studies of sleep and learning have demonstrated that training on various tasks increases subsequent rapid eye movement (REM) sleep and phasic pontine-wave (P-wave) activity, followed by improvement in performance on the learned task. It is well documented that REM sleep deprivation after learning trials blocks the expected improvement in performance on subsequent retesting. Our aim was to test whether experimentally induced P-wave generator activation could eliminate the learning impairment produced by post-training REM sleep deprivation. Rats were trained on a two-way active avoidance-learning task. Immediately thereafter, two groups of those rats received a control vehicle (100 nl saline) microinjection and one group received a carbachol (50 ng in 100 nl saline) microinjection into the P-wave generator. The carbachol-injected group and one of the two control saline microinjected groups were selectively deprived of REM sleep during a 6 hr polygraphic recording session. All rats were then tested on the avoidance-learning task. The rats that received both the control saline injection and REM sleep deprivation showed learning deficits compared with the control saline-injected rats that were allowed to sleep normally. In contrast, the rats that received the carbachol microinjection and REM sleep deprivation demonstrated normal learning. These results demonstrate, for the first time, that carbachol-induced activation of the P-wave generator prevents the memory-impairing effects of post-training REM sleep deprivation. This evidence supports our hypothesis that the activation of the P-wave generator during REM sleep deprivation enhances a physiological process of memory, which occurs naturally during post-training REM sleep.

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Section: Effects Of Rem Sleep Deprivation On Learning Performancesupporting

confidence: 90%

Activation of Phasic Pontine-Wave Generator Prevents Rapid Eye Movement Sleep Deprivation-Induced Learning Impairment in the Rat: A Mechanism for Sleep-Dependent Plasticity

Datta¹,

Mavanji²,

Ulloor³

et al. 2004

J. Neurosci.

150

167

View full text Add to dashboard Cite

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“…Each method has associated positives and negatives and has been discussed more thoroughly previously (see Havekes et al 2012). Sleep deprivation administered after learning disrupts the consolidation period and impairs memories (Fishbein 1971;Leconte et al 1974;Linden et al 1975). The hippocampus, in particular, appears to be vulnerable to this manipulation, as demonstrated in hippocampal-dependent memory tasks after sleep deprivation.…”

Section: Sleep Deprivation Disrupts Memory Consolidationmentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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“…Around the same time that experimental studies began to suggest a role for sleep in memory consolidation (Fishbein, 1971;Pearlman and Greenberg, 1973; but see Siegel, 2001), Marr (1971) proposed that, during periods such as sleep, when the brain is not occupied with the processing of ongoing events (i.e., "off-line"), spontaneous reactivation of memory traces in the hippocampus may initiate and coordinate a process of information retrieval and repeated transfer within the neocortex, leading to the stabilization and refinement of the cortical memory trace. Contemporary studies have supported the notion of spontaneous, temporally specific replay of firing patterns in hippocampal area CA1 during postexperiential sleep and rest states (Pavlides and Winson, 1989;Wilson and McNaughton, 1994;Skaggs and McNaughton, 1996;McNaughton, 1998;Kudrimoti et al, 1999;Louie and Wilson, 2001).…”

Section: Introductionmentioning

confidence: 99%

The Ventral Striatum in Off-Line Processing: Ensemble Reactivation during Sleep and Modulation by Hippocampal Ripples

et al. 2004

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Previously it has been shown that the hippocampus and neocortex can spontaneously reactivate ensemble activity patterns during post-behavioral sleep and rest periods. Here we examined whether such reactivation also occurs in a subcortical structure, the ventral striatum, which receives a direct input from the hippocampal formation and has been implicated in guidance of consummatory and conditioned behaviors. During a reward-searching task on a T-maze, flanked by sleep and rest periods, parallel recordings were made from ventral striatal ensembles while EEG signals were derived from the hippocampus. Statistical measures indicated a significant amount of reactivation in the ventral striatum. In line with hippocampal data, reactivation was especially prominent during postbehavioral slow-wave sleep, but unlike the hippocampus, no decay in pattern recurrence was visible in the ventral striatum across the first 40 min of post-behavioral rest. We next studied the relationship between ensemble firing patterns in ventral striatum and hippocampal ripples-sharp waves, which have been implicated in pattern replay. Firing rates were significantly modulated in close temporal association with hippocampal ripples in 25% of the units, showing a marked transient enhancement in the average response profile. Strikingly, ripple-modulated neurons in ventral striatum showed a clear reactivation, whereas nonmodulated cells did not. These data suggest, first, the occurrence of pattern replay in a subcortical structure implied in the processing and prediction of reward and, second, a functional linkage between ventral striatal reactivation and a specific type of high-frequency population activity associated with hippocampal replay.

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Disruptive effects of rapid eye movement sleep deprivation on long-term memory

Cited by 130 publications

References 20 publications

Activation of Phasic Pontine-Wave Generator Prevents Rapid Eye Movement Sleep Deprivation-Induced Learning Impairment in the Rat: A Mechanism for Sleep-Dependent Plasticity

Activation of Phasic Pontine-Wave Generator Prevents Rapid Eye Movement Sleep Deprivation-Induced Learning Impairment in the Rat: A Mechanism for Sleep-Dependent Plasticity

The impact of sleep loss on hippocampal function

The Ventral Striatum in Off-Line Processing: Ensemble Reactivation during Sleep and Modulation by Hippocampal Ripples

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