The Contribution of Sleep to Hippocampus-Dependent Memory Consolidation

University of Lübeck, Department of Neuroendocrinology, Haus 23a, Ratzeburger Allee 160, 23538 Lübeck, Germany.
Trends in Cognitive Sciences (Impact Factor: 21.97). 11/2007; 11(10):442-50. DOI: 10.1016/j.tics.2007.09.001
Source: PubMed


There is now compelling evidence that sleep promotes the long-term consolidation of declarative and procedural memories. Behavioral studies suggest that sleep preferentially consolidates explicit aspects of these memories, which during encoding are possibly associated with activation in prefrontal-hippocampal circuitry. Hippocampus-dependent declarative memory benefits particularly from slow-wave sleep (SWS), whereas rapid-eye-movement (REM) sleep seems to benefit procedural aspects of memory. Consolidation of hippocampus-dependent memories relies on a dialog between the neocortex and hippocampus. Crucial features of this dialog are the neuronal reactivation of new memories in the hippocampus during SWS, which stimulates the redistribution of memory representations to neocortical networks; and the neocortical slow (<1Hz) oscillation that synchronizes hippocampal-to-neocortical information transfer to activity in other brain structures.

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Available from: Lisa Marshall, Dec 23, 2014
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    • "Neuroimaging studies across the lifespan have targeted the hippocampus to understand how sleep quantity and physiology contribute to learning and memory. Work in young adults has demonstrated that sleep is essential to hippocampal-dependent learning (Yoo et al., 2007; Marshall and Born, 2007; Van Der Werf et al., 2009; Nguyen et al., 2013; for review see: Abel et al., 2013). "
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    ABSTRACT: Older adults experience parallel changes in sleep, circadian rhythms, and episodic memory. These processes appear to be linked such that disruptions in sleep contribute to deficits in memory. Although more variability in circadian patterns is a common feature of aging and predicts pathology, little is known about how alterations in circadian activity rhythms within older adults influence new episodic learning. Following 10 days of recording sleep-wake patterns using actigraphy, healthy older adults underwent fMRI while performing an associative memory task. The results revealed better associative memory was related to more consistent circadian activity rhythms, independent of total sleep time, sleep efficiency, and level of physical activity. Moreover, hippocampal activity during successful memory retrieval events was positively correlated with associative memory accuracy and circadian activity rhythm (CAR) consistency. We demonstrated that the link between consistent rhythms and associative memory performance was mediated by hippocampal activity. These findings provide novel insight into how the circadian rhythm of sleep-wake cycles are associated with memory in older adults and encourage further examination of circadian activity rhythms as a biomarker of cognitive functioning. Copyright © 2015. Published by Elsevier Ltd.
    Neuropsychologia 07/2015; 75. DOI:10.1016/j.neuropsychologia.2015.07.020 · 3.30 Impact Factor
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    • "Recent research suggests that sleep benefits memory consolidation (Maquet, 2001; Rasch & Born, 2007; Stickgold, 2005). A large body of evidence indicates that sleep promotes both declarative and procedural memory consolidation in various tasks (Marshall & Born, 2007; Smith, 2001; Walker, Brakefield, Hobson, & Stickgold, 2003). Compared with an equal duration of wakefulness, post-learning sleep enhances the retention of declarative memory and improves performance in procedural skills (Plihal & Born, 1997; Walker et al., 2003). "
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    ABSTRACT: Recent research has used context cues (odor or auditory cues) to target memories during sleep and has demonstrated that they can enhance declarative and procedural memories. However, the effects of external cues re-presented during sleep on emotional memory are still not fully understood. In the present study, we conducted a Pavlovian fear conditioning/extinction paradigm and examined the effects of re-exposure to extinction memory associated contextual tones during slow-wave sleep (SWS) and wakefulness on fear expression. The participants underwent fear conditioning on the first day, during which colored squares served as the conditioned stimulus (CS) and a mild shock served as the unconditioned stimulus (US). The next day, they underwent extinction, during which the CSs were presented without the US but accompanied by a contextual tone (pink noise). Immediately after extinction, the participants were required to take a nap or remain awake and randomly assigned to six groups. Four of the groups were separately exposed to the associated tone (i.e. SWS-Tone group and Wake-Tone group) or an irrelevant tone (controltone, CtrT) (i.e. SWS-CtrT group and Wake-CtrT group), while the other two groups were not (i.e. SWS-No Tone group and Wake-No Tone group). Subsequently, the conditioned responses to the CSs were tested to evaluate the fear expression. All of the participants included in the final analysis showed successful levels of fear conditioning and extinction. During the recall test, the fear responses were significantly higher in the SWS-Tone group than that in the SWS-No Tone group or the SWS-CtrT group, while the Wake-Tone group exhibited more attenuated fear responses than either the Wake-No Tone group or Wake-CtrT group. Otherwise, re-exposure to auditory tones during SWS did not affect sleep profiles. These results suggested that distinct conditions during which re-exposure to an extinction memory associated contextual cue contributes to differential effects on fear expression. Copyright © 2015. Published by Elsevier Inc.
    Neurobiology of Learning and Memory 06/2015; 123. DOI:10.1016/j.nlm.2015.06.005 · 3.65 Impact Factor
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    • "These effects might be due to the disturbances in the levels of brain monoamines,. In accordance, several studies indicated that sleep is involved in learning and memory processes [34] [42] [43]. Support for this theory comes from experiments showing the importance of sleep after learning, and the deleterious effect of sleep deprivation on subsequent learning [44] [45]. "
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    ABSTRACT: The present study focused on investigating the possible neuroprotective potential of peripheral glibenclamide pretreatment and sleep recovery on sleep deprivation effects in rats and the possible mechanisms of action (s). Adult male rats were sleep deprived for a period of 3 days using grid suspended over water method. Morris water maze was used to reveal the effect of both sleep deprivation and the different treatments on learning and memory. Potential mechanisms were explored applying HPLC-UV determination of hippocampal and cortical monoamines in rats. In addition, blood brain barrier intergrity was determined in different groups using Evans blue dye extravasation method. Sleep deprivation induced learning impairment and learning deterioration and neuromotor deficit. The concentrations of 5-hydroxytryptamine (5-HT), norepinephrine (NE) and dopamine (DA) significantly decreased in both brain cortex and hippocampus after sleep deprivation Moreover, sleep deprivation increased blood brain barrier permeability and induced extravasation of the Evans Blue dye in the tested brain areas. Glibenclamide pretreatment antagonized sleep deprivation-induced learning impairment and learning deterioration, and neuromotor deficit. However, pre-treatments with glibenclamide significantly increased the concentrations of 5-HT and NE in rat cortex and hippocamps and minmized the blood brain barrier permeabilty. Moreover, recovery sleep for 48 hours remarkably antagonized sleep-adverse effects. These changes might suggest that the neurochemical changes and the impairment of blood brain barrier function are-at least partly-the underlying mechanism of adverse effects of sleep deprivation on memory and learning. In addition, the potective and restorative effects of glibenclamide and sleep recovery, respectively, against sleep deprivation might be mediated through rebalance the brain chemistry and restoring the normal function of blood brain barrier.
    Journal of Global Biosciences 05/2015; 4(4):1971-1981.
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