Four hours of paradoxical sleep deprivation impairs alternation performance in a water maze in the rat

Sixteen rats were deprived of paradoxical sleep (PS) for 4 h using the "flower pot" technique and 16 other served as yoked controls. PS-deprived and control rats then had to learn a water maze using either a standard allocentric configuration (i.e., finding the submerged platform using external cues; n = 6/group) or an alternation version (goal platform alternating between two locations; n 10/group). Rats were submitted to six trials with a cutoff time of 60 s and an intertrial interval of 5 min. Criterion was set as two consecutive successful completions. PS-deprived rats made more quadrant entries and took more time to reach criterion on the alternation task than control rats while both groups were equal on the allocentric task. Based on lesion studies (Ethier et al., this issue) we propose that tasks that require an intact medial prefrontal cortex are particularly sensitive to PS deprivation.     

Perinatal linoleate deprivation impairs learning and memory in adult rats

Rats receiving polyunsaturated fatty acid (PUFA) deficient diets during the perinatal period showed in adult age undisturbed acquisition of a footshock motivated brightness discrimination task, but a significant impairment of retention. The same effects on retention were obtained in rats receiving the PUFA deficient diet in adulthood, when the behavioral parameters were investigated at the end of the dietary treatment.     

Twenty-four hours of total sleep deprivation selectively impairs attentional networks

Performance decrements after sleep loss have been extensively studied and are usually attributed to generic attentional deficits. This claim, however, is based on the view of attention as a unitary construct, despite evidence that it should be considered a multidimensional cognitive ability. The aim of the present study was to evaluate the impact of one night of sleep deprivation on the efficiency of three attentional networks, defined by Posner and Raichle (1994) in anatomical and functional terms, as alerting, orienting, and executive control. Thirty participants performed the Attention Network Test at 9:00 a.m. following two different sleep conditions: baseline (a normal night of sleep) and deprivation (24 hrs of wakefulness). Results showed an overall slowing in reaction times and a significant decrease in accuracy after sleep deprivation. Sleep deprivation selectively affected the three attentional networks, given that only executive control efficacy significantly decreased after sleep deprivation. By contrast, phasic alerting and orienting showed no differences in the two sleep conditions. Thus, performance deficits following sleep deprivation do not reflect global attentional deficits.     

Sleep deprivation selectively impairs memory consolidation for contextual fear conditioning

Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0–5 and 5–10 h after training for contextual and cued fear conditioning. We found that sleep deprivation from 0–5 h after training for this task impaired memory consolidation for contextual fear conditioning whereas sleep deprivation from 5–10 h after training had no effect. Sleep deprivation at either time point had no effect on cued fear conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for fear conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage.     

Effects of sleep deprivation on short-term recognition memory.

A probe-recognition short-term memory paradigm was used to inquire into the precise effects of sleep deprivation on human memory. It was found that recognition performance, as measured by d', was generally impaired for each subjects after 24 hr of sleep deprivation. While d' was shown to decrease exponentially as the number of items intervening between the target and the probe increased, this decay rate was not affected by sleep loss. In addition there was confirmation of a previously observed increase in the positive skewness of reaction times after wakefulness. The data were consistent with the hypothesis that sleep deprivation increases the occurrence of lapses, periods of lowered reactive capacity, which prevent the encoding of items in short-term memory.     

When two is too many: Collaborative encoding impairs memory

Humans routinely encode and retrieve experiences in interactive, collaborative contexts. Yet much of what we know about human memory comes from research on individuals working in isolation. Some recent research has examined collaboration during retrieval, but not much is known about how collaboration during encoding affects memory. We examined this issue. Participants created episodes by elaborating on study materials alone or collaboratively, and they later performed a cued-recall task alone, with the study partner, or with a different partner (Experiment 1). Collaborative encoding impaired recall. This counterintuitive outcome was found for both individual and group recall, even when the same partners collaborated across encoding and retrieval. This impairment was significantly reduced, but persisted, when the encoding instructions encouraged free-flowing collaboration (Experiment 2). Thus, the collaborative-encoding deficit is robust in nature and likely occurs because collaborative encoding produces less effective cues for later retrieval.     

Effects of sleep deprivation on auditory and visual memory tasks

Probe recognition tasks have shown the effects of sleep deprivation following a full night of sleep loss. The current study investigated shorter durations of deprivation by testing 11 subjects for accuracy and response time every 2 hr. from 10 p.m. through 8 a.m. We replicated Elkin and Murray's auditory single-probe recognition task using the number triplets and added two visual tasks with number and shape triplets. Series of six stimuli were each followed by a probe, which was presented after 2.5 sec. as a short delay or 20 sec. as a long delay. Accuracy performance showed a significant decrease for the long delay beginning after 4 a.m. for the two visual tasks. Response times were significantly slower for the visual shapes task using the short delay. Visual tasks, especially shapes, may be more prone to disruption by sleep deprivation, given the visual information load and the briefness of iconic memory.     

Total sleep deprivation increases the costs of shifting between simple cognitive tasks

In two experiments we studied the effects of one night of total sleep deprivation on task-shift costs. In different conditions shifts were between types of judgment (extradimensional shifts) and between stimulus-response mappings (intradimensional shifts). In addition, with an alternating-runs procedure we used short and long response-to-stimulus intervals and also external precues to vary the opportunities for advance configuration of task sets. Under all conditions sleep deprivation increased shift costs derived from the 20% slowest reaction times, which were insensitive to the opportunities for advance configuration. Shift costs derived from the 20% fastest reaction times were increased only for extradimensional shifts. As indicated by congruency effects, the increase of shift costs after a night without sleep cannot be attributed to increased interference between competing task sets. The findings suggest that total sleep deprivation increases task-set instability and thus lapsing, in particular in conditions with long stimulus-to-response intervals and in shift trials. In addition total sleep deprivation seems to increase the duration of an exogenously controlled process involved in extradimensional shifts.     

The influence of sleep deprivation and knowledge of results on perceptual encoding

This study investigates the way sleep deprivation effects on perceptual processes are modulated by knowledge of results (KR). In a choice-reaction task, signal quality was manipulated, combined with and without KR and under increasing levels of lack of sleep. It was found that the decrease of performance due to sleep deprivation was larger when stimuli were degraded. KR counteracted the effect of sleep deprivation; however, KR improved performance irrespective of signal quality. Hence, sleep deprivation seems to have a twofold effect on performance; one effect on perceptual processing, which is insensitive to KR, and another effect on some different processing stage, which is sensitive to KR. The results were interpreted in terms of a model of human performance (Sanders 1983) in which a distinction is made between two energetical mechanisms, ‘arousal’ and ‘activation’, subserving perceptual and motor stages of information processing, respectively. Thus, KR appears to compensate for the deficiency of one type of energetical mechanism, caused by sleep deprivation. Yet, this compensation does not appear to be the result of increased arousal, because, irrespective of KR, the performance decrement caused by signal degradation was more pronounced with lack of sleep.     

Avoidance performance in rat enhanced by postlearning paradoxical sleep deprivation

This series of experiments investigates possible relations between increases in paradoxical sleep (PS), persisting for several days after an avoidance training, and improvement of retention performance that occurred 3 days following partial training in a brightness discrimination Y-maze shock-avoidance task. Sprague-Dawley rats were trained in the Y-maze and PS deprived for 24 h either immediately or 24, 48, or 72 h following initial training. Contrary to what was expected, the results indicated that PSD immediately following the training session enhanced the avoidance performance after a 7-day retention interval. PSD at later times had no effect. Experiment 2 indicated that this effect was obtained only for PS-deprived animals and not for those placed in the PSD situation, but on larger platforms. Thus enhancement of the avoidance performance was not due to increases in stress or arousal caused by PSD-associated factors. Experiment 3 showed that the facilitative effect of a non-delayed 24-h PSD was obtained immediately thereafter as well as 24 h later, demonstrating that this effect was not due to any PS rebound which might have occurred following the PSD. Alternative explanations for these unexpected results are discussed.     

Paradoxical sleep deprivation impairs acquisition, consolidation, and retrieval of a discriminative avoidance task in rats

The aim of the present study was to investigate the effects of paradoxical sleep deprivation (PSD) for 96 h on the learning/memory processes in rats submitted to the plus-maze discriminative avoidance task (PM-DAT), which simultaneously evaluates learning, memory, anxiety and motor function. Four experiments were performed in which rats were submitted to: (1) post-training and pre-test PSD; (2) post-training or pre-test PSD; (3) pre-training PSD or pre-training paradoxical sleep (PS) rebound (24 h) and (4) pre-test PSD rebound. Concerning Experiment I, post-training and pre-test PSD induced memory deficits, an anxiolytic-like behavior and an increase in locomotor activity. In Experiment II, both post-training PS-deprived and pre-test PS-deprived groups showed memory deficits per se. However, only the pre-test PS-deprived animals presented anxiolytic-like behavior and increased locomotor activity. In Experiment III, pre-training PS-deprived rats showed learning and memory deficits, anxiolytic-like behavior and increased locomotor activity. A 24h-sleep recovery period after the PSD abolished the learning and memory deficits but not anxiety and locomotor alterations. Finally, sleep rebound did not modify acquisition (Experiment III) and retrieval (Experiment IV). This study strengthened the critical role of paradoxical sleep (but not sleep rebound) in all the phases of learning and memory formation. In addition, it suggests that PSD effects on acquisition and consolidation do not seem to be related to other behavioral alterations induced by this procedure.     

Activation of adenosine receptors in the posterior cingulate cortex impairs memory retrieval in the rat

Adenosine A1 and A2A receptor agonists and antagonists have been reported to alter learning and memory. The aim of our study was to investigate the involvement of adenosinergic system in memory retrieval into posterior cingulate cortex (PCC) of Wistar rats. To clarify this question, we tested specifics agonist and antagonists of adenosine A1 and A2A receptors in rats submitted to a one-trial inhibitory avoidance task. The stimulation of adenosine A1 and A2A receptors by CPA and CGS21680, respectively, impaired memory retrieval for inhibitory avoidance task, into PCC. These findings provide behavioral evidence for the role of adenosinergic system in the memory retrieval into PCC.     

Sleep deprivation impairs object recognition in mice

Many studies in animals and humans suggest that sleep facilitates learning, memory consolidation, and retrieval. Moreover, sleep deprivation (SD) incurred after learning, impaired memory in humans, mice, rats, and hamsters. We investigated the importance of sleep and its timing in an object recognition task in OF1 mice subjected to 6h SD either immediately after the acquisition phase (0-6 SD) or 6h later (7-12 SD), and in corresponding undisturbed controls. Motor activity was continuously recorded with infrared sensors. All groups explored two familiar, previously encountered objects to a similar extent, both at the end of the acquisition phase and 24h later during the test phase, indicating intact familiarity detection. During the test phase 0-6 SD mice failed to discriminate between the single novel and the two familiar objects. In contrast, the 7-12 SD group and the two control groups explored the novel object significantly longer than the two familiar objects. Plasma corticosterone levels determined after SD did not differ from time-matched undisturbed controls, but were significantly below the level measured after learning alone. ACTH did not differ between the groups. Therefore, it is unlikely that stress contributed to the memory impairment. We conclude that the loss of sleep and the activities the mice engaged in during the SD, impaired recognition memory retrieval, when they occurred immediately after acquisition. The delayed SD enabled memory consolidation during the 6h when the mice were allowed to sleep, and had no detrimental effect on memory. Neither SD schedule impaired object familiarity processing, suggesting that only specific cognitive abilities were sensitive to the intervention. Sleep may either actively promote memory formation, or alternatively, sleep may provide optimal conditions of non-interference for consolidation.     

The effects of total sleep deprivation on recognition memory processes: A study of event-related potential

This study examined the memorization of information after a night of normal sleep and total sleep deprivation (TSD) by means of event-related potentials (ERPs). We expected a disfacilitatory effect of TSD on memory processing. Eighteen subjects were tested twice in a counterbalanced fashion. During the study session, subjects were presented with unfamiliar face stimuli and asked to memorize them for a subsequent memory test. At the test session, the subjects were presented with the studied faces intermixed with “new” faces and asked to indicate the previously presented stimuli. The N100 was used as a covariate to control for the differences in level of vigilance between the two sessions. Sleep deprivation decreased subjects’ ability to discriminate new from previously studied stimuli and decreased the peak amplitude of the early component (N200) to the decrement of performance. In addition, following TSD the amplitude of the late frontal component (LFC), which is thought to reflect contextual processing, was decreased in covariance with the N100 vigilance component. The amplitude of the late posterior component (LPC/P600) was also reduced but was unrelated to the vigilance component of the ERP. Based on prior studies, this LPC reduction can be interpreted to indicate a decrease in information retrieved after TSD. In summary, a night of TSD decreased the amplitude of the ERPs associated with complex episodic memory task stimuli, affected the frontal cortex during episodic retrieval, and prevented the elaboration process. Furthermore, there was an inability to discriminate what is and what is not in memory, possibly due to less local processing of details.     

Spatial learning on the Morris Water Maze Test after a short-term paradoxical sleep deprivation in the rat

Twelve rats were deprived of paradoxical sleep (PS) for eight hours using the small platform method. PS-deprived and control rats then learned either the standard allocentric version (using external cues) of the Morris Water Maze (MWM) or a delayed alternation version (changing the platform location between trials: MWM(DA)). Overall, rats learning the MWM(DA) made more quadrant entries than rats learning the allocentric version. Compared to other rats, PS-deprived rats crossed more quadrants only in the MWM(DA). These results show that MWM(DA) is a more complex task to learn and is more vulnerable to PS deprivation than allocentric spatial orientation. Since delayed alternation is dependent upon frontal structures, we propose that tasks involving the frontal cortex are more sensitive to short-term PS deprivation than tasks related to hippocampal structures.     

Effects of pre- or post-training paradoxical sleep deprivation on two animal models of learning and memory in mice

The aim of the present study was to verify the effects of pre- or post-training paradoxical sleep (PS) deprivation in mice tested in the passive and the plus-maze discriminative avoidance tasks. Three-month-old Swiss male mice were placed in narrow platforms in a water tank for 72 h to prevent the occurrence of PS. Control animals were kept in the same room, but in their home cages. Before or after this period, the animals were submitted to the training session of one of the behavioral tasks. The test sessions were performed 3 and 10 days after the training. The animals that were PS-deprived before the training session showed retention deficits in the test sessions performed 3 days later in both tasks (decreased latency to enter the dark chamber of the passive avoidance apparatus or increased percent time spent in the aversive arm of the plus-maze discriminative avoidance apparatus). Animals that were PS deprived after the training session showed no differences from control animals in the test sessions performed 3 days after the training in any of the tasks, but showed passive and discriminative avoidance retention deficits in the test performed 10 days after the training. The results suggest that both pre- and post-training paradoxical sleep deprivation produce memory deficits in mice. However, these effects have different temporal characteristics.     

Inhibition and working memory: effect of acute sleep deprivation on a random letter generation task]

The literature contains inconsistent data on the effects of acute sleep deprivation on the superior cognitive functions. The primary purpose of this study is to determine the effectiveness of inhibition, one of the functions of the working memory executive centre (EC), over an extended, 36-hour waking period. Inhibition is a cognitive mechanism whereby individuals ignore non-relevant information recorded in their working memory. We also tested the effects of a 36-hour period of acute sleep deprivation on simple reaction time. Twelve young, healthy volunteers (M = 21.5 years, sigma = 2.3) performed a random generation task involving letters and a simple reaction time psychomotor test over four sessions held at 10-hour intervals. Each participant was assigned a "constant routine." Participants were kept awake in a prone position within a room whose environment was held strictly constant (light, noise, temperature, meals, etc.). This control procedure provided assurance that any variation in participant performance was solely caused by sleep deprivation. The random generation task, nearly two minutes in length, consisted in verbally producing a sequence of 100 letters in a random fashion (i.e. by inhibiting, for example, alphabetical order) and by keeping to a set rhythm. Our assumption was that capacity for inhibition diminished as the number of hours of sleep deprivation increased. The simple reaction test, 10 minutes in length, involved pressing a button as swiftly as possible to cause a black square to disappear from a screen. In this case our assumption was that acute sleep deprivation alters simple reaction time. Analysis of variance (ANOVA) through repeated measures using the "sessions" factor as an intra-subject variable showed no significant changes in randomization indices of the random generation task, contrary to analysis of average simple reaction times. Participants' reaction times deteriorated over the first two minutes of the test during the night they were deprived of sleep. It would seem that the contradictory results of previous studies of the effects of acute sleep deprivation on the inhibition function would be due to errors in factor identification. In conclusion, the inhibition function, as measured during the performance of a brief task, seems to remain intact during an extended, 36-hour waking period. Simple reaction time assessed by means of a brief psychomotor test is affected during a night of sleep deprivation. The working-memory inhibition executive function shows greater resistance to acute sleep deprivation than does psychomotor reaction time for the performance of short tasks.     

Inhibition of return impairs episodic memory access

The term inhibition of return (IOR) refers to a bias against returning attention to a location or object that has recently been attended. The effect has been shown to occur in various perceptual tasks including stimulus detection, localization, and discrimination, but also to affect higher cognitive processes like lexical access. The present experiments examined whether inhibition of return would impair the high-level processing that is required in accessing item representations in episodic memory. The results show that reaction times for recognition memory decisions are increased under IOR. Furthermore, IOR affects the accuracy of recognition memory, and this effect interacts with the ease of memory access, manipulated, for example, by encoding depth in the learning phase. These results suggest that IOR impairs attentional processing up to the highest cognitive levels, including the access of prior item encounters in episodic memory.     

Inhibition of return impairs episodic memory access

The term inhibition of return (IOR) refers to a bias against returning attention to a location or object that has recently been attended. The effect has been shown to occur in various perceptual tasks including stimulus detection, localization, and discrimination, but also to affect higher cognitive processes like lexical access. The present experiments examined whether inhibition of return would impair the high-level processing that is required in accessing item representations in episodic memory. The results show that reaction times for recognition memory decisions are increased under IOR. Furthermore, IOR affects the accuracy of recognition memory, and this effect interacts with the ease of memory access, manipulated, for example, by encoding depth in the learning phase. These results suggest that IOR impairs attentional processing up to the highest cognitive levels, including the access of prior item encounters in episodic memory.