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Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2020) 32 (9): 1688–1703.
Published: 01 September 2020
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Sleep enhances memories, especially if they are related to future rewards. Although dopamine has been shown to be a key determinant during reward learning, the role of dopaminergic neurotransmission for amplifying reward-related memories during sleep remains unclear. In this study, we scrutinize the idea that dopamine is needed for the preferential consolidation of rewarded information. We impaired dopaminergic neurotransmission, thereby aiming to wipe out preferential sleep-dependent consolidation of high- over low-rewarded memories during sleep. Following a double-blind, balanced, crossover design, 17 young healthy men received the dopamine d2-like receptor blocker sulpiride (800 mg) or placebo, after learning a motivated learning task. The task required participants to memorize 80 highly and 80 lowly rewarded pictures. Half of them were presented for a short (750 msec) and a long (1500 msec) duration, respectively, which permitted dissociation of the effects of reward on sleep-associated consolidation from those of mere encoding depth. Retrieval was tested after a retention interval of approximately 22 hr that included 8 hr of nocturnal sleep. As expected, at retrieval, highly rewarded memories were remembered better than lowly rewarded memories, under placebo. However, there was no evidence for an effect of reducing dopaminergic neurotransmission with sulpiride during sleep on this differential retention of rewarded information. This result indicates that dopaminergic activation likely is not required for the preferential consolidation of reward-associated memory. Rather, it appears that dopaminergic activation only tags such memories at encoding for intensified reprocessing during sleep.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2014) 26 (10): 2310–2320.
Published: 01 October 2014
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Memory formation is a selective process in which reward contingencies determine which memory is maintained and which is forgotten. Sleep plays a pivotal role in maintaining information for the long term and has been shown to specifically benefit memories that are associated with reward. Key to memory consolidation during sleep is a neuronal reactivation of newly encoded representations. However, it is unclear whether preferential consolidation of memories associated with reward requires the reactivation of dopaminergic circuitry known to mediate reward effects at encoding. In a placebo-controlled, double-blind, balanced crossover experiment, we show that the dopamine D2-like receptor agonist pramipexole given during sleep wipes out reward contingencies. Before sleep, 16 men learned 160 pictures of landscapes and interiors that were associated with high or low rewards, if they were identified between new stimuli at retrieval 24 hr later. In the placebo condition, the participants retained significantly more pictures that promised a high reward. In the pramipexole condition, this difference was wiped out, and performance for the low reward pictures was as high as that for high reward pictures. Pramipexole did not generally enhance memory consolidation probably because of the fact that the dopaminergic agonist concurrently suppressed both SWS and REM sleep. These results are consistent with the concept that preferential consolidation of reward-associated memories relies on hippocampus-driven reactivation within the dopaminergic reward system during sleep, whereby during sleep reward contingencies are fed back to the hippocampus to strengthen specific memories, possibly, through dopaminergic facilitation of long-term potentiation.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2014) 26 (8): 1806–1818.
Published: 01 August 2014
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Memories are reactivated during sleep. Re-exposure to olfactory cues during sleep triggers this reactivation and improves later recall performance. Here, we tested if the effects of odor-induced memory reactivations are odor-specific, that is, requiring the same odor during learning and subsequent sleep. We also tested whether odor-induced memory reactivation affects oscillatory EEG activity during sleep, as a putative mechanism underlying memory processing during sleep. Participants learned a visuospatial memory task under the presence of an odor. During subsequent SWS, the same odor, a different odor, or an odorless vehicle was presented. We found that odor re-exposure during sleep significantly improves memory only when the same odor was presented again, whereas exposure to a new odor or the odorless vehicle had no effect. The memory-enhancing effect of the congruent odor was accompanied by significant increases in frontal delta (1.5–4.5 Hz) and parietal fast spindle (13.0–15.0 Hz) power as well as by an increased negative-to-positive slope of the frontal slow oscillation. Our results indicate that odor-induced memory reactivations are odor specific and trigger changes in slow-wave and spindle power possibly reflecting a bottom–up influence of hippocampal memory replay on cortical slow oscillations as well as thalamo-cortical sleep spindles.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2012) 24 (1): 119–132.
Published: 01 January 2012
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The number reduction task (NRT) allows us to study the transition from implicit knowledge of hidden task regularities to explicit insight into these regularities. To identify sleep-associated neurophysiological indicators of this restructuring of knowledge representations, we measured frequency-specific power of EEG while participants slept during the night between two sessions of the NRT. Alpha (8–12 Hz) EEG power during slow wave sleep (SWS) emerged as a specific marker of the transformation of presleep implicit knowledge to postsleep explicit knowledge (ExK). Beta power during SWS was increased whenever ExK was attained after sleep, irrespective of presleep knowledge. No such EEG predictors of insight were found during Sleep Stage 2 and rapid eye movement sleep. These results support the view that it is neuronal memory reprocessing during sleep, in particular during SWS, that lays the foundations for restructuring those task-related representations in the brain that are necessary for promoting the gain of ExK.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2011) 23 (12): 3703–3712.
Published: 01 December 2011
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Memory functions involve three stages: encoding, consolidation, and retrieval. Modulating effects of glucocorticoids (GCs) have been consistently observed for declarative memory with GCs enhancing encoding and impairing retrieval, but surprisingly, little is known on how GCs affect memory consolidation. Studies in rats suggest a beneficial effect of GCs that were administered during postlearning wake periods, whereas in humans, cortisol impaired memory consolidation when administered during postlearning sleep. These inconsistent results raise the question whether effects of GCs critically depend on the brain state during consolidation (sleep vs. wake). Here, we compare for the first time directly the effects of cortisol on memory consolidation during postlearning sleep and wakefulness in different measures of declarative memory. Cortisol (13 mg vs. placebo) was intravenously infused during a postlearning nap or a time-matched period of wakefulness after participants had encoded neutral and emotional text material. Memory for the texts was tested (a) by asking for the contents of the texts (“item” memory) and (b) for the temporal order of the contents within the texts (“relational” memory). Neither postlearning infusion of cortisol during sleep nor during wakefulness affected retention of content words of emotional or neutral texts. Critically, however, the retention of temporal order within the texts, known to rely most specifically on the hippocampus proper within the medial-temporal lobe memory system, was distinctly improved by cortisol infusion during the wake phase but impaired by cortisol during sleep. These results point toward fundamentally different mechanisms of hippocampal memory consolidation, depending on the brain state.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2011) 23 (9): 2582–2592.
Published: 01 September 2011
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There is a long-standing assumption that low noradrenergic activity during sleep reflects mainly the low arousal during this brain state. Nevertheless, recent research has demonstrated that the locus coeruleus, which is the main source of cortical noradrenaline, displays discrete periods of intense firing during non-REM sleep, without any signs of awakening. This transient locus coeruleus activation during sleep seems to occur in response to preceding learning-related episodes. In the present study, we manipulate noradrenergic activity during sleep in humans with either the α2-autoreceptor agonist clonidine or the noradrenaline reuptake inhibitor reboxetine. We show that reducing noradrenergic activity during sleep, but not during wakefulness, impairs subsequent memory performance in an odor recognition task. Increasing noradrenergic availability during sleep, in contrast, enhances memory retention. We conclude that noradrenergic activity during non-REM sleep interacts with other sleep-related mechanisms to functionally contribute to off-line memory consolidation.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2011) 23 (4): 772–781.
Published: 01 April 2011
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Retrieving a memory is a reconstructive process in which encoded representations can be changed and distorted. This process sometimes leads to the generation of “false memories,” that is, when people remember events that, in fact, never happened. Such false memories typically represent a kind of “gist” being extracted from single encountered events. The stress hormone cortisol is known to substantially impair memory retrieval. Here, in a double-blind, placebo-controlled crossover design, we tested the effect of an intravenous cortisol infusion before retrieval testing on the occurrence of false memories and on recall of correct memories using a modified Deese–Roediger–McDermott paradigm. Subjects studied sets of abstract shapes, with each set being derived from one prototype that was not presented during learning. At retrieval taking place 9 hr after learning, subjects were presented with studied shapes, nonstudied shapes, and the prototypes, and had to indicate whether or not each shape had been presented at learning. Cortisol administration distinctly reduced susceptibility to false memories (i.e., false recognition of prototypes) and, in parallel, impaired retrieval of correct memories (i.e., correct recognition of studied shapes). Response bias as well as confidence ratings and remember/know/guess judgments were not affected. Our results support gist-based theories of false memory generation, assuming a simultaneous storage of the gist and specific details of an event. Cortisol, by a general impairing influence on retrieval operations, decreases, in parallel, retrieval of false (i.e., gist) and correct (i.e., specific) memories for the event.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2007) 19 (2): 214–227.
Published: 01 February 2007
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Sleep crucially contributes to the off-line consolidation of memories. Although this view was confirmed in numerous studies in adults, it is not known whether it can be generalized to sleep during development. Here, we examined effects of sleep on implicit memory formation considered of particular relevance in children, because brain structures underlying implicit learning develop earlier in ontogeny than structures supporting explicit learning. Subjects were 7- to 11-year-old children ( n = 14) and 20- to 30-year-old adults ( n = 12) tested on a serial reaction time task before (learning) and after (retest) equal length retention periods of overnight sleep and daytime wakefulness. At learning, after eight training blocks, all subjects had acquired implicit knowledge of the probabilistic rules underlying the sequential stimulus materials, as indicated by a substantial difference in response time to grammatical versus nongrammatical trials in two test blocks that followed the training blocks. At learning, this response time difference was greater in children (48.49 ± 6.08 msec) than adults (28.02 ± 3.65 msec, p < .01), but did not differ between sleep and wake retention conditions in either age group. Consistent with previous studies, retesting in the adults revealed that the reaction time differences between grammatical and nongrammatical trials increased by 9.78 ± 4.82 msec after sleep, but decreased by −12.76 ± 5.49 msec after the wake retention period ( p < .01). Contrary to this finding in adults, sleep in children did not lead to an increase, but to a decrease in the reaction time difference averaging −26.68 ± 12.25 msec ( p < .05), whereas across the wake retention interval the reaction time difference remained nearly unchanged. The sleep-dependent deterioration in measures of implicit sequence knowledge in children was in striking contrast to the gain of such knowledge in the adults during sleep ( p < .01). Our findings indicate that the functional role of sleep in implicit memory consolidation depends on age. We speculate that the overnight decrease of implicit knowledge in children reflects a preferential effect of sleep toward the enhancement of explicit aspects of task performance that interferes with implicit performance gains.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2006) 18 (5): 793–802.
Published: 01 May 2006
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High central nervous system levels of acetylcholine (ACh) are commonly regarded as crucial for learning and memory, and a decline in cholinergic neurotransmission is associated with Alzheimer's dementia. However, recent findings revealed exceptions to this rule: The low ACh tone characterizing slowwave sleep (SWS) has proven necessary for consolidation of hippocampus-dependent declarative memories during this sleep stage. Such observations, together with recent models of a hippocampal-neocortical dialogue underlying systems memory consolidation, suggest that high levels of ACh support memory encoding, whereas low levels facilitate consolidation. We tested this hypothesis in human subjects by blocking cholinergic neurotransmission during wakefulness, starting 30 min after learning. Subjects received the muscarinic antagonist scopolamine (4 µg/kg bodyweight intravenously) and the nicotinic antagonist mecamylamine (5 mg orally). Compared to placebo, combined muscarinic and nicotinic receptor blockade significantly improved consolidation of declarative memories tested 10 hr later, but simultaneously impaired acquisition of similar material. Consolidation of procedural memories, which are not dependent on hippocampal functioning, was unaffected. Neither scopolamine nor mecamylamine alone enhanced declarative memory consolidation. Our findings support the notion that ACh acts as a switch between modes of acquisition and consolidation. We propose that the natural shift in central nervous system cholinergic tone from high levels during wakefulness to minimal levels during SWS optimizes declarative memory consolidation during a period with no need for new memory encoding.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2006) 18 (3): 311–319.
Published: 01 March 2006
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There is evidence that sleep supports the enhancement of implicit as well as explicit memories (i.e., two memory systems that during learning normally appear to act together). Here, employing a serial reaction time task (SRTT) paradigm, we examined the question whether sleep can provide explicit knowledge on an implicitly acquired skill. At learning, young healthy subjects ( n = 20) were first trained on the SRTT. Then, implicit knowledge was assessed on two test blocks, in which grammatically incorrect target positions were occasionally interspersed by the difference in reaction times between grammatically correct and incorrect target positions. To assess explicit sequence knowledge, thereafter subjects performed on a generation task in which they were explicitly instructed to predict the sequential target positions. In half the subjects, learning took place before a 9-hour retention interval filled with nocturnal sleep (sleep group), in the other half, the retention interval covered a 9-hour period of daytime wakefulness (wake group). At subsequent retesting, both testing on the generation task and the SRTT test blocks was repeated. At learning before the retention interval, subjects displayed significant implicit sequence knowledge which was comparable for the sleep and wake groups. Moreover, both groups did not display any explicit sequence knowledge as indicated by a prediction performance not differing from chance on the generation task. However, at retesting, there was a distinct gain in explicit knowledge in the subjects who had slept in the retention interval, whereas generation task performance in the wake group remained at chance level. SRTT performance in the test blocks at retesting did not indicate any further gain in skill (i.e., unchanged reaction time differences between grammatically correct and incorrect target positions) independently of whether subjects had slept or remained awake after learning. Our results indicate a selective enhancement of explicit memory formation during sleep. Because before sleep subjects only had implicit knowledge on the sequence of target transitions, these data point to an interaction between implicit and explicit memory systems during sleep-dependent off-line learning.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (1997) 9 (4): 534–547.
Published: 01 July 1997
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Recall of paired-associate lists (declarative memory) and mirror-tracing skills (procedural memory) was assessed after retention intervals defined over early and late nocturnal sleep. In addition, effects of sleep on recall were compared with those of early and late retention intervals filled with wakefulness. Twenty healthy men served as subjects. Saliva cortisol concentrations were determined before and after the retention intervals to determine pituitary-adrenal secretory activity. Sleep was determined somnopolygraphically. Sleep generally enhanced recall when compared with the effects of corresponding retention intervals of wakefulness. The benefit from sleep on recall depended on the phase of sleep and on the type of memory: Recall of paired-associate lists improved more during early sleep, and recall of mirror-tracing skills improved more during late sleep. The effects may reflect different influences of slow wave sleep (SWS) and rapid eye movement (REM) sleep since time in SWS was 5 times longer during the early than late sleep retention interval, and time in REM sleep was twice as long during late than early sleep ( p < 0.005). Changes in cortisol concentrations, which independently of sleep and wakefulness were lower during early retention intervals than late ones, cannot account for the effects of sleep on memory. The experiments for the first time dissociate specific effects of early and late sleep on two principal types of memory, declarative and procedural, in humans.