Declarative memory consolidation during the first night in a sleep lab: The role of REM sleep and cortisol.
ABSTRACT While the consolidation of declarative memory is supported by slow wave sleep (SWS) in healthy subjects, it has been shown to be associated with rapid eye movement (REM) sleep in patients with insomnia. Sleep during a subject's first night in an unfamiliar environment is often disturbed, and this so-called first-night effect (FNE) has often been used as a model of transient insomnia. Additionally, sleeping for the first time in an unfamiliar environment can lead to increased cortisol secretion, and declarative memory consolidation likely depends on low cortisol levels, especially during the early part of the night. Accounting for intersubject variability in the FNE, we examined the relationship between sleep stages, cortisol secretion and declarative memory performance in 27 healthy young men. Declarative memory performance improved significantly after sleep. Whereas memory performance during the learning session and retrieval testing was strongly associated with cortisol secretion, the overnight gain was not. Post hoc analyses indicated that the overnight gain appears to be modulated by the extent of the FNE: a significant overnight improvement in memory performance was found only in subjects with a weak FNE (n=12). In these subjects, no association was found between any sleep stage and the improvement observed in their memory performance. In subjects with a strong FNE (n=12), however, the overnight change in memory performance was associated with the proportion of REM sleep and the total number of REMs. Disturbed sleep in an unfamiliar environment therefore appears to affect the memory consolidation process.
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ABSTRACT: 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.Learning & memory (Cold Spring Harbor, N.Y.) 09/2013; 20(10):558-69. DOI:10.1101/lm.031674.113 · 4.08 Impact Factor
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ABSTRACT: Transient global amnesia (TGA) is a temporary memory loss characterized by an abrupt onset of antero-grade and retrograde amnesia, totally reversible. Since sleep plays a major role in memory consolidation, and in the storage of memory-related traces into the brain cortex, the aims of the present study were: (1) to evaluate changes in sleep macro-structure in TGA; (2) to assess modifications in sleep micro-structure in TGA, with particular reference to the arousal EEG and to cyclic alternating pattern (CAP); (3) to compare sleep parameters in TGA patients with a control group of patients with acute ischemic events ("minor stroke" or transient ischemic attack [TIA]) clinically and neuroradiologically "similar" to the TGA. TGA GROUP: 17 patients, (8 men and 9 women, 60.2 ± 12.5 years). Stroke or TIA (SoT) group: 17 patients hospitalized in the Stroke Unit for recent onset of minor stroke or TIA with hemispheric localization; healthy controls (HC) group: 17 healthy volunteers, matched for age and sex. Patients and controls underwent full-night polysomnography. In the multivariate analysis (conditions TGA, SoT, and HC) a significant effect of the condition was observed for sleep efficiency index, number of awakenings longer 1 min, REM latency, CAP time, and CAP rate. TGA and SoT differed only for CAP time and CAP rate, which were lower in the TGA group. MICROSTRUCTURAL MODIFICATION ASSOCIATED WITH TGA COULD BE CONSEQUENT TO: (1) hippocampal dysfunction and memory impairment; (2) impairment of arousal-related structures (in particular, cholinergic pathways); (3) emotional distress. Della Marca G; Mazza M; Losurdo A; Testani E; Broccolini A; Frisullo G; Marano G; Morosetti R; Pilato F; Profice P; Vollono C; Di Lazzaro V. Sleep modifications in acute transient global amnesia. J Clin Sleep Med 2013;9(9):921-927.Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 09/2013; 9(9):921-7. DOI:10.5664/jcsm.2994 · 2.93 Impact Factor
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ABSTRACT: Rapid eye movement (REM) sleep is considered critical to the consolidation of procedural memory - the memory of skills and habits. Many antidepressants strongly suppress REM sleep, however, and procedural memory consolidation has been shown to be impaired in depressed patients on antidepressant therapy. As a result, it is important to determine whether antidepressive therapy can lead to amnestic impairment. We thus investigated the effects of the anticholinergic antidepressant amitriptyline on sleep-dependent memory consolidation. Double-blind, placebo-controlled, randomized, parallel-group study. Sleep laboratory. Twenty-five healthy men (mean age: 26.8 ± 5.6 y). 75 mg amitriptyline versus placebo. To test memory consolidation, a visual discrimination task, a finger-tapping task, the Rey-Osterrieth Complex Figure Test, and the Rey Auditory-Verbal Learning Test were performed. Sleep was measured using polysomnography. Our findings show that amitriptyline profoundly suppressed REM sleep and impaired perceptual skill learning, but not motor skill or declarative learning. Our study is the first to demonstrate that an antidepressant can affect procedural memory consolidation in healthy subjects. Moreover, considering the results of a recent study, in which selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors were shown not to impair procedural memory consolidation, our findings suggest that procedural memory consolidation is not facilitated by the characteristics of REM sleep captured by visual sleep scoring, but rather by the high cholinergic tone associated with REM sleep. Our study contributes to the understanding of potentially undesirable behavioral effects of amitriptyline. Goerke M, Cohrs S, Rodenbeck A, Kunz D. Differential effect of an anticholinergic antidepressant on sleep-dependent memory consolidation. SLEEP 2014;37(5):977-985.Sleep 05/2014; 37(5):977-985. DOI:10.5665/sleep.3674 · 5.06 Impact Factor