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Sleep and memory I: The influence of different sleep stages on memory
Abstract
A new approach to the sleep stages role in memory is discussed in the context of the two opposite patterns of behavior-search activity and renunciation of search. Search activity is activity designed to change the situation (or the subjects attitudes to it) in the absence of a definite forecast of the results of such activity, but with the constant consideration of these results at all stages of activity. Search activity increases general adaptability and body resistance while renunciation of search decreases adaptability and requires REM sleep for its compensation. Unprepared learning, which is often accompanied by failures on the first steps of learning, is suggested to produce renunciation of search, which decreases learning ability, suppress retention, and increase REM sleep requirement. A prolonged REM sleep deprivation before training causes learned helplessness and disturbs the learning process, while short REM sleep deprivation cause the "rebound" of the compensatory search activity that interferes with passive avoidance. REM sleep deprivation performed after a training session can increase distress caused by a training procedure, with the subsequent negative outcome on retention.
... How can mental recombination be functional within the economy of the nervous system? Following a line of thinking that dreams possess adaptive psychological function (Cohen, 1979;Greenberg & Pearlman, 1974;Palambo, 1978;Rotenberg, 1992aRotenberg, , 1992bRotenberg, , 1996, we suggest that dreaming, as mental recombination, serves as a counterpoint to the waking tendency towards context (e.g. habit, rote, expectation) formation. ...
... Increased REM duration following unprepared learning seems to support some role of REM in the consolidation process (Rotenberg, 1996). However, Rotenberg's arguments that increased REM following unprepared learning is due to anxiety reduction mechanisms not necessarily related to memory consolidation cannot be lightly dismissed (Rotenberg & Arshavsky 1979;Rotenberg 1992aRotenberg , 1992b. ...
... (1988), this paper compares conscious and unconscious processes across waking, nonlucid, and lucid dreams. Sleep psychology can display gross functional dissociation between perceptual and cognitive consciousness. We utilize this observation to develop models of sleep experience and dream generation. These models accommodate Hunt’s (1989) “multiplicity of dreams”, as well as the intrinsic variation of perceptual and cognitive activity during dreaming. Lucid dreams are suggested to result from the presence of a skill-based mental set, the lucid dream context, which allows voluntary interaction with the spontaneous dream process. Our view of dreaming provides an explanation of the tendency of lucid dreams to either fade or revert to nonlucid dreams. Neurobiological considerations lead us to hypothesize that, in the sleeping brain, a reversal of information flow from medial temporal lobe mnemonic structures to thalamocortical perceptual circuits imparts parameterization to dream perceptual consciousness. A consequence of our thinking is that dreaming results in a “mental recombination” of cerebral information networks, which contributes to the ability of waking consciousness to generate novel and adaptive
... In spite of its deep implications, the association between the production of LH and SD consequences has received limited attention. Although several investigators have addressed the relationships between REM sleep and depression using inescapable footshock to produce LH as a model of depression, 11 only two reports have proposed that SD could be in fact a cause of LH. 12,13 It has been argued that the lesions produced after long-term SD and LH (and any other stress-mediated procedure) are different. 14 For instance, SD caused hyperphagia, ulcers in paws and tail and deep thermoregulatory disturbances. ...
... However, it has been argued that these differences are a result of the methodological differences between SD and LH. 12,13 For instance, in normal LH, the punishment is always applied during waking, whereas, in SD, the punishment only occurs after effective sleep entrance. The normal waking behaviour is suppressed in LH, whereas this is not the case in SD, which causes overactivity of waking behaviours such as feeding. ...
Rest in poikilothermic animals is an adaptation of the organism to adjust to the geophysical cycles, a doubtless valuable function for all animals. In this review, we argue that the function of sleep could be trivial for mammals and birds because sleep does not provide additional advantages over simple rest. This conclusion can be reached by using the null hypothesis and parsimony arguments. First, we develop some theoretical and empirical considerations supporting the absence of specific effects after sleep deprivation. Then, we question the adaptive value of sleep traits by using non-coding DNA as a metaphor that shows that the complexity in the design is not a definitive proof of adaptation. We then propose that few, if any, phenotypic selectable traits do exist in sleep. Instead, the selection of efficient waking has been the major determinant of the most significant aspects in sleep structure. In addition, we suggest that the regulation of sleep is only a mechanism to enforce rest, a state that was challenged after the development of homeothermy. As a general conclusion, there is no direct answer to the problem of why we sleep; only an explanation of why such a complex set of mechanisms is used to perform what seems to be a simple function. This explanation should be reached by following the evolution of wakefulness rather than that of sleep. Sleep could have additional functions secondarily added to the trivial one, although, in this case, the necessity and sufficiency of these sleep functions should be demonstrated.
... Numerous studies imply that memory and learning are influenced by sleep on a variety of levels. Some research demonstrates that REM sleep enhances memory, while others reveal that the beginning part of the night with slow-wave sleep (SWS) significantly impacts memory consolidation (1). Memory and learning are closely related to stress, and chronic and acute stress can also affect sleep structure and circadian rhythms (2). ...
Objective(s)
Three physiological processes interact: sleep, learning, and stress. It is essential to understand how stress affects and interacts with the link between sleep, learning, and memory since it has long been recognized that sleep plays a crucial role in memory consolidation and learning. Through naloxone injection in the baso lateral amygdala (BLA), this study intends to shed light on the interactions between stress, learning, and sleep, as well as the function of the opioid system and its impact on brain-derived neurotrophic factor (BDNF) production in the hippocampus.
Materials and Methods
Male Wistar rats (n=77) in eleven groups were implanted with electroencephalogram (EEG) and electromyography (EMG) recording electrodes, and the BLA area was bilaterally cannulated. Recordings of Rapid Eye Movement (REM) and Non-Rapid Eye Movement (NREM) sleep and wakefulness steps were made for the three hours prior to and three hours following the implementation of the immobility stress protocol and learning with the Barnes maze for three consecutive days. Also, the animals’ memory was tasted 48 hr later. Before the stress and learning procedure, naloxone was injected into each BLA three times in a row at a dosage of 0.05 μg or 0.1 μg in a volume of 0.5 μl. A molecular biomarker of learning and stress, BDNF, was also examined.
Results
The study demonstrated that the immobility stress model lowers REM and NREM sleep. On the other hand, putting the learning technique into practice results in more REM and NREM sleep, and stress situations do not stop this rise after learning. Naloxone injections in the BLA region also enhance learning and memory, preventing stress-related REM and NREM sleep loss. Additionally, stress lowers BDNF expression in the hippocampal region. BDNF expression rises in the hippocampus throughout the learning process, and naloxone administration in the BLA area also raises BDNF expression in the hippocampus.
Conclusion
Stress generally reduces REM, NREM, and BDNF expression in the hippocampal region. Under stress, using the learning protocol increases REM, NREM sleep, and BDNF. Naloxone injection in BLA improves memory and learning, reducing stress-induced memory loss.
... It is of interest to point out that the action that melatonin has on the sleep of our patients could have therapeutic benefits on memory and learning deficits, characteristic of AD, especially for the performance of this tasks the day following the administration of the drug, because it has been proved that REM sleep and phase 2 non-REM sleep are closely related to different cognitive processes which are underneath memory and learning fixation and maintenance. [32][33][34] Additionally, during REM sleep, cell restoration processes that are not observed in any other moment during the sleep-wake cycle take place. On the other side, it is of interest to point out that the secretion of growth hormones and the synthesis of neurotrophins 21 both take place during delta sleep; these processes of physiological restoration are very important in AD. 35 It has been suggested that sleep is controlled by two systems. ...
The objective of the-present study was to evaluate the 5 mg. melatonin effects on the sleep macro-architecture in eight patients with middle to moderate Alzheimer's disease (DTA). Using the polysomnographic technique (PSG), we made a simple-blind, non-randomized, controlled with placebo study. The PSG was carried out according to the following order: night 1: placebo administration; night 2 and 3: continues melatonin administration. In the first night with melatonin treatment, the sleep latency to the first episode of Stage 2, Delta and REM sleep, was significantly diminished as compared with placebo (<= .05). No significant difference in total time of each sleep stage and sleep efficiency was observed. Nevertheless, a tendency to diminish the total time of nocturnal wake and increase of the total sleep time in the second night with melatonin treatment was observed. We conclude that melatonin can improve sleep in patients with middle to moderate DTA.
... Es de interés señalar que la acción que ejerce la melatonina sobre el sueño de nuestros pacientes podría tener beneficios terapéuticos sobre el déficit de memoria y aprendizaje característicos de la DTA, sobre todo para el desempeño de estas funciones al día siguiente de haber administrado el fármaco, ya que se ha demostrado que el sueño MOR y la fase 2 del sueño no-MOR se encuentran estrechamente relacionados con distintos procesos cognitivos que subyacen a la fijación y mantenimiento de la memoria y el aprendizaje. [32][33][34] Asimismo, durante el sueño MOR tienen lugar procesos de restauración celular que no se observan en ningún otro momento del ciclo sueño-vigilia. Por otro lado, es de interés señalar que durante el sueño delta tienen lugar la secreción de hormona de crecimiento y la síntesis de neurotrofinas, 21 procesos de restauración fisiológica que son sumamente importantes en la DTA. ...
El objetivo del presente estudio fue determinar los efectos de 5 mg.
de melatonina de liberación inmediata sobre la macro-arquitectura
del sueño en ocho pacientes con diagnóstico de Demencia Tipo
Alzheimer (DTA) de media a moderada. Utilizando la técnica polisomnográfica
(PSG) se realizó un estudio simple ciego, no aleatorio,
controlado con placebo. Los registros PSG se llevaron a cabo de la
siguiente manera: Noche 1: administración de placebo; noche 2 y 3:
administración continua de melatonina (5 mg). Observamos que el
tratamiento con melatonina durante la primera noche de administración
disminuyó significativamente la latencia de la fase 2, del sueño
de ondas delta y el sueño de MOR al ser comparadas con el placebo
(P ≤.05). No se observaron diferencias significativas en el tiempo
total de cada fase de sueño; tampoco se observaron diferencias en
la eficiencia del sueño en presencia de la melatonina. Sin embargo
se observó una tendencia a la disminución del tiempo total de vigilia
y un aumento del tiempo total de sueño, principalmente durante la
segunda noche de tratamiento. Concluimos que la melatonina puede
mejorar el sueño en pacientes con DTA de media a moderada.
... Different authors have proposed that REM sleep is a necessary state for the consolidation of short-and long-term memory, given that the deprivation of REM sleep causes failures and losses in memory and therefore learning. [77][78][79][80][81] On the other hand, learning tasks increase REM sleep and the number of REMs for two to three days after the completion of a task, both in animals and in humans. 82,83 From a neurophysiological point of view, it is still difficult to explain the strange sensations, discontinuousness, incoherence, and incongruousness of dreams. ...
Understanding the phenomenon of sleep and dreams has always fascinated
humans. However, the scientific study of sleep is relatively
recent. In 1953, Aserinsky and Kleitman found that slow wave sleep
(SWS) was periodically interrupted by episodes of rapid EEG activity,
which are accompanied by rapid eye movements (REMs), and named
this sleep phase as REM sleep. Subsequently in 1957, Dement and
Kleitman discovered that these rapid eye movements coincided with
the appearance of dreams. By using experimental animal models,
the subcortical mechanisms underlying REM sleep have been studied,
and it has been demonstrated that this activity depends on the serotonergic
activity from wakefulness, which promotes the formation of
peptides that trigger certain structures of the brainstem, where cholinergic
mechanisms of REM sleep are integrated. In turn, on the pontine
region monophasic phasic potentials (300-400 μV) are generated
that can also be recorded on the lateral geniculate body and in the
occipital cortex, hence the name of ponto-geniculo-occipital waves
(PGO). These potentials spread to the oculomotor system to provoke
the REMs of REM sleep and possibly give rise to visual hallucinatory
phenomena. Furthermore, it has been shown that certain limbic structures
related to emotion and memory are activated by these potentials.
This suggests that PGO waves generate mnemonic and emotional
components of dreams. Several aspects of the functions of these PGO
waves remain to be determined, but knowledge about the origin of
brain phenomena that generate dreams has had a breakthrough from
its study. In this present work we review the literature concerning the
work done on PGO waves and its contribution to the knowledge of the
origin and functions of dreams.
... Cuando se labora durante el Rev Fac Med UN Col 2001 Vol 49 N°2 día con una computadora y llega el momento de irse a descansar, se escogen los archivos que se han de eliminar, se empiezan a organizar los que se van a utilizar al día siguiente, se guardan otros en el disco duro para su uso posterior, es decir, se organiza la información usada durante el día. Se plantea un paralelo con el sueño MOR, es decir, durante el día el ser humano presenta comportamientos y pensamientos que se organizarían durante el dormir teniendo en cuenta la interacción genes -medio ambiente (6, 17,18). Esta hipótesis es bastante aceptada en la actualidad. ...
Sleep disorders are a frequent pathology. Nearly 35% Colombians will have a sleep disorder at any time in their lives. Insomnia is the main complaint in adults and the elderly.
... Sin embargo, a pesar de numerosos descubrimientos en este campo, en la actualidad de la función del sueño poco se sabe. De todas maneras se plantean las funciones reparadora, adaptativa, homeostática y de consolidación de algunas funciones cognoscitivas, según se trate de una u otra de las dos grandes fases del dormir: el estado de sueño no MOR o MOR (14), (15), (16), (17), (18). ...
Sleep physiology and its neuroanatomic basis is currently only partially clarified. We know the modifications sleep can suffer but not its function, so it is postulated that its principal role is to repair and regulate the central nervous system and other structures of the body. Hypersomnia represents a frequent problem with a global prevalence of around 16%. It is an important symptom for both the patient and his companion, and the approach to the diagnosis includes complete auto and heteroanamnesis. Also, subjective and objective methods exist that facilitate the diagnosis and allow the etiology to be clarified. Somatic, psychological exams (Epworth Sleepiness Scale, Stanford Sleepiness Scale), polysomnography, as well as multiple sleep latency tests and maintenance of wakefulness tests are used. Chronic sleep deprivation syndrome, hypersomnia associated with sleep-disordered breathing or sleep apnea, motor dysfunctions during sleep, narcolepsy and idiopathic hypersomnia, among others, are frequent causes of hypersomnia. An appropriate intervention demands careful diagnosis and an etiological treatment.
... Distintos autores han propuesto que el sueño MOR es un estado necesario para la consolidación de la memoria de corto y de largo plazo, ya que la privación del sueño MOR provoca fallas y errores en la memoria y por lo tanto también del aprendizaje. [77][78][79][80][81] Por otra parte, las tareas de aprendizaje incrementan el sueño MOR y el número de MORs durante dos a tres días posteriores a la realización de la tarea, tanto en animales como en el hombre. 82,83 Desde un punto de vista neurofisiológico aún es difícil explicar la sensación de extrañeza, lo discontinuo y lo incoherente e incongruente de los sueños. ...
El fenómeno del sueño y de los sueños es algo que siempre ha fascinado
al hombre. Sin embargo, el estudio científico del sueño es relativamente
reciente. En 1953, Aserinsky y Kleitman encontraron que el sueño de
ondas lentas (SOL) es interrumpido periódicamente por episodios de
actividad EEG rápida, que se acompañan de movimientos oculares rápidos
(MORs), y denominaron a esta fase “sueño MOR”. Posteriormente,
Dement y Kleitman, en 1957, descubrieron que estos movimientos
oculares rápidos coinciden con la aparición de los sueños. Utilizando
animales de experimentación se han estudiado los mecanismos subcorticales
que subyacen al sueño MOR y se ha demostrado que éste
depende de una actividad serotoninérgica de la vigilia, que promueve
la formación de péptidos que ponen en marcha ciertas estructuras de la
región pontina del tallo cerebral en donde se integran los mecanismos
colinérgicos del sueño MOR. En la región pontina, a su vez, se generan
potenciales monofásicos de alto voltaje (300-400 μV) que también pueden
registrarse en el cuerpo geniculado lateral y en la corteza occipital,
de allí el nombre de potenciales ponto-genículo-occipitales (PGO). Estos
potenciales se propagan hacia el sistema oculomotor para provocar
los MORs y posiblemente den origen a los fenómenos oníricos visuales.
Además se ha demostrado que ciertas estructuras del sistema límbico,
relacionadas con las emociones y la memoria, son activadas por dichos
potenciales. Lo anterior sugiere que los potenciales PGO generan los
componentes mnésicos y emocionales de los sueños. Quedan aún por
determinarse varios aspectos sobre las funciones de estos potenciales,
pero el conocimiento sobre el origen de los fenómenos cerebrales que
generan los sueños ha tenido un gran avance a partir de su estudio. En
el presente artículo se revisa la bibliografía concerniente a los trabajos
realizados sobre los potenciales PGO y su aportación al conocimiento
del origen y las funciones de los sueños.
... It is of interest to point out that the action that melatonin has on the sleep of our patients could have therapeutic benefits on memory and learning deficits, characteristic of AD, especially for the performance of this tasks the day following the administration of the drug, because it has been proved that REM sleep and phase 2 non-REM sleep are closely related to different cognitive processes which are underneath memory and learning fixation and maintenance. [32][33][34] Additionally, during REM sleep, cell restoration processes that are not observed in any other moment during the sleep-wake cycle take place. On the other side, it is of interest to point out that the secretion of growth hormones and the synthesis of neurotrophins 21 both take place during delta sleep; these processes of physiological restoration are very important in AD. 35 It has been suggested that sleep is controlled by two systems. ...
The objective of the present study was to evaluate the 5 mg. melatonin
effects on the sleep macro-architecture in eight patients with middle
to moderate Alzheimer´s disease (DTA). Using the polysomnographic
technique (PSG), we made a simple-blind, non-randomized, controlled
with placebo study. The PSG was carried out according to the following
order: night 1: placebo administration; night 2 and 3: continues
melatonin administration. In the first night with melatonin treatment, the
sleep latency to the first episode of Stage 2, Delta and REM sleep, was
significantly diminished as compared with placebo (≤.05). No significant
difference in total time of each sleep stage and sleep efficiency
was observed. Nevertheless, a tendency to diminish the total time of
nocturnal wake and increase of the total sleep time in the second night
with melatonin treatment was observed. We conclude that melatonin
can improve sleep in patients with middle to moderate DTA.
... It is possible to suggest that REM sleep is especially important for the animal during the critical period of an acute conversion from the previous stereotypical behavior to the new style of beha- vior. It might be a sign that REM sleep plays only an indirect role in the process of retention by carrying out its main function – compensation of renunciation of search and restoration of search activity (Rotenberg, 1992). A complex problem that the subject is not ready to solve, a difficult task that requires unprepared learning may cause renunciation of search with much greater probability than a simple one, especially at the early stages of the solution when failures prevail over successes. ...
Search activity concept provides a new classification of the behavior which distinguishes search activity (activity in the uncertain situation with the constant feedback between behavior and its outcome), stereotyped behavior with a definite probability forecast, panic (activity without feedback between activity and its outcome) and renunciation of search. Only search activity which includes fight, flight, orienting behavior and creativity raises the body's resistance to stress, to nat- ural and experimentally induced pathology whereas renunciation of search which display itself in freezing, helplessness and depression forms a nonspecific predisposition to somatic disturbances (e.g. psychosomatic diseases). Dreams in REM sleep are regarded as a specific form of search activity aimed at compensating for the lack of search in waking. REM sleep deprivation on a small as well as on rotating platform raises the requirement in REM sleep by frustrating search activity. It is suggested that in wakefulness characterized by the prominent search activity the inhibitory alpha-2- adrenoreceptors became less sensitive to stimulation and consequently in this state the activity of the brain monoamine neurons is less limited by the level of brain monoamines. During renunciation of search brain monoamine synthesis is not stimulated by monoamine exhaustion. In REM sleep the critical level of brain monoamines for search activity to start is lower than in wakefulness and alpha-2-adrenoreceptors are less sensitive than in the state of renunciation of search although more sensitive than during search behavior in waking. REM sleep indirectly contributes to memory consolida- tion by carrying out its main function - restoration of search activity. A functionally sufficient REM sleep contains search activity in dreams (subject is active in his/her own dream scenario) while in functionally insufficient REM sleep dreams are characterized by subject's passive position and feeling of helplessness. REM sleep insufficiency is an obligate condition for mental and somatic disorders to appear. The difference between normal (adaptive) and pathological (mala- daptive) emotional tension is determined by the presence or absence of search activity in the structure of emotional ten- sion. Repression of the unacceptable motive causing neurotic anxiety is a human variant of renunciation of search. Hy- pochondriac symptoms are in negative relationships with psychosomatic disorders and they, as well as positive symp- toms in schizophrenia and anorectic behavior in anorexia nervosa, represent a pathological misdirected search activity.
... Insomnia and self-neglect are a direct expression of renunciation of search. Impaired memory seems to be an indirect effect of renunciation of search [154,155]. Similarly, the levels of 5-HT are lower among recent depressive suicide attempters than among non-suicidal depressed people [98]. Thus, these suicides are characterized by a more extreme renunciation of search than in other cases of depression. ...
This paper presents an integrative approach to suicidal behavior in terms of search activity concept. Search activity concept displays a broad and holistic approach to behavior, adaptation to environment, body resistance, brain amine metabolism, and REM-sleep functions. Search activity is defined as activity that is oriented to change the situation (or at least the subject's attitude to it) in the absence of a precise prediction of the outcome of such activity, but taking into consideration outcomes at all previous stages of activity. According to the proposed hypothesis, renunciation of search (a state opposed to search activity) leads to a feeling of helplessness, problem-solution deficits, inefficient coping, dreams that represent renunciation of search, and a drop in the activity of amines. All these factors further exacerbate the state of renunciation of search and elevate suicidal risk. In addition, the remnants of search activity are misdirected to self-defeating behaviors that increase mental pain and contribute to renunciation of search. This hypothesis integrates findings from a number of fields of study of suicidal behavior, resolves some paradoxes, suggests new lines of research, and raises suggestions for assessment and treatment of suicidal behavior.
Fish oil (FO) is one of the richest natural sources of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). DHA is essential for brain functions and EPA has been approved for brain health. On the other hand, stathmin, TFEB, synaptophysin and LAMP-1 proteins are involved in synaptic plasticity, lysosome biogenesis and synaptic vesicles biogenesis. In this study, we aimed to investigate the effect of FO on social interaction memory in sleep-deprived rats with respect to level of stathmin, TFEB, synaptophysin and LAMP-1 in the hippocampus of rats. All rats received FO through oral gavage at the doses of 0.5, 0.75 and 1 mg/kg. The water box was used to induce total sleep deprivation (TSD) and the three-chamber paradigm test was used to assess social behavior. Hippocampal level of proteins was assessed using Western blot. The results showed, FO impaired social memory at the dose of 1 mg/kg in normal and sham groups. SD impaired social memory and FO did not restore this effect. Furthermore, FO at the dose of 0.75 mg/kg decreased social affiliation and social memory in all groups of normal rats, compared with related saline groups, and at the dose of 1 mg/kg impaired social memory for stranger 2 compared with saline group. In sham groups, FO at the dose of 1 mg/kg impaired social memory for stranger 2 compared with saline group. SD decreased hippocampal level of all proteins (except stathmin), and FO (1 mg/kg) restored these effects. In conclusion, FO negatively affects social interaction memory in rats.
By combining neurobiological data with facts and ideas from psychology psychiatry and quantum mechanics, a new, multidisciplinary view is presented on the relationship between, and the origin of, brain and mind. This view, summarized in six propositions, substantially deviates from leading contemporary theories on this subject. Particular consequences of this view are that, from the very beginning, cosmic evolution is characterized by superdeterminism and, secondly, that by far the greater part of unconscious mental activity, including the storage of declarative memories, does not physically occur in the synaptic networks of the material brain but at a deeper, submanifest level. Propositions 1. The electrochemical functioning of the cerebral cortex, on the one hand, and the related subjective experiences, on the other, are two fundamentally different, but really existing and intimately related, equivalent, self-organizing phenomena: an objective-material and a subjective-psychic one. 2. The continuously changing deterministic chaotic electric/magnetic fields (virtual photons) along the dendritic trees in the cerebral cortex can partly be boasted to such complex, highly ordered time-spatial patterns that the latter give rise to subjective experiences (psychic functioning) including self-consciousness. 3. The whole, self-organizing, course of the universe, extending over the past, present and future, is in its relevant space-time configuration (causal and acausal) permanently present in a submanifest order of being. From this submanifest order of being, a small part continually actualizes itself via a continuous succession of quantum states and interactions in the manifest order of being. We experience this advancing, propagating present as the course of everyday life. 4. The electric/magnetic fields generated in the material cerebral cortex, on the one hand, and the corresponding psychic functioning, on the other, are two fundamentally different, but equivalent aspects of one and the same, self-organizing, energetic entity which, with the maintenance of both aspects, has its roots in a deeper submanifest order of being. 5. A retrieved declarative memory is nothing but a transient re-actualization in the functioning cerebral cortex of information arising from the unconsciousness located in a personal domain of the submanifest order of being. Thus, unconscious mental activity, including the storage of declarative memories, does not physically occur in the synaptic networks of the cerebral cortex or elsewhere in the brain, but somewhere in a personal domain of the submanifest order of being. 6. Each subjectively perceptible psychic process, such as a sensory perception, thought, emotion, dream, hallucination or memory, on the one hand, and the associated objectively perceptible electric/magnetic fields in the cerebral cortex, on the other, should be regarded as two different, but equivalent and intimately related aspects of one and the same self-organizing structure, which has been formed as a certain acausal configuration in space and time from a submanifest order of being in which everything that was, is, or is still to come, is enclosed (contained) in 'mutual reflection'. This submanifest order of being can be subdivided into a personal and a collective domain which are in line with each other.
Samples consisting of 10 patients out of each of the following diagnostic groups are compared to each other, as well as to a selected control group, with regard to their sleep polygram: narcisssistic depression resp. MDD, schizophrenia, psychosomatic and borderline disease and anorexia nervosa. The different and common aspects of the standard parameters of sleep (quantitative proportions of the sleep stages) and the parameters of structure (segmentation of time) are illustrated in a synopsis. Furthermore the authors attempt to compare the sleep structure of individual diseases with those of other diseases and with those of the selected control group in terms of delimitative entities. On the background of sleep sturctures, which also entails comparisons of ectreme groups with regard to the allocation of NREM 3 and the length of REM latency, the attempt is made to investigate how far aspects of sleep structure coincide with aspects of human-structure as described by Ammon, on the basis of his human-structural concept with respect to the various psychiatric diseases.
Normal sleep is required for optimal functioning. Normal wakefulness should be effortless and free of unintended sleep episodes. Problem sleepiness is common and occurs when the quantity of sleep is inadequate because of primary sleep disorders, other medical conditions or lifestyle factors. Medications and substances that disturb sleep, such as caffeine and nicotine, or those that have sedating side effects, may also cause problem sleepiness. This condition can lead to impairment in attention, performance problems at work and school, and potentially dangerous situations when the patient is driving or undertaking other safety-sensitive tasks. However, problem sleepiness is generally correctable when it iS recognized. Asking a patient and his or her bed partner about the likelihood of drowsiness or of falling asleep during specific activities, as well as questions that uncover factors contributing to the sleepiness, helps the physician to recognize the disorder. Accurate diagnosis of specific sleep disorders may require evaluation by a specialist. The primary care physician is in an ideal position to identify signs and symptoms of problem sleepiness and initiate appropriate care of the patient, including educating the patient about the dangers of functioning while impaired by sleepiness.
Samenvatting In nogal wat gevalsstudies over de effecten van Eye Movement Desensitization (emd) wordt geclaimd dat emd het visuele geheugen
ondermijnt. De suggestie is dat dit effect wel eens ten grondslag zou kunnen liggen aan de gunstige uitwerking van emd. In
deze laboratoriumstudie werd nagegaan of emd inderdaad een negatief effect heeft op het visuele geheugen. Normale proefpersonen
zagen een reeks van dia's, waaronder een aversieve dia. Vervolgens kregen de proefpersonen de opdracht om zich de dia's in
herinnering te brengen. Inmiddels werd de ene helft met emd en de andere helft met een controle–interventie ‘behandeld’. Daarna
werd de proefpersonen gevraagd zoveel mogelijk dia's te reproduceren. emd bleek niet te leiden tot een verminderde reproductie.
Ook was er geen enkele aanwijzing dat emd speciaal het geheugen voor de aversieve dia negatief had beïnvloed. De resultaten
worden in een bredere context geplaatst.
Selection of hypnotics for drug formularies in The Netherlands, France and the UK is made by means of the System of Objectified Judgement Analysis (SOJA) method. The following criteria are included in the method: clinical efficacy (maximal 300 points), adverse effects (250 points), clinical documentation (150 points), cost (120 points), pharmacokinetic properties (80 points), toxicity (50 points), drug interactions (30 points) and the number of tablet strengths available (20 points). In all 3 countries, zolpidem, zopiclone and temazepam showed the highest score, followed by lormetazepam. High scores favour inclusion in formularies. Nitrazepam and loprazolam scored 75 to 130 points less than the top 3, and flunitrazepam shows the lowest score (119 to 183 points less than zolpidem, zopiclone and temazepam). Therefore, the first 3 (or 4) hypnotics are most suitable for formulary inclusion while the others are not.
Biological structures can be seen as collections of special devices coordinated by a matrix of organization. Devices are dif?cult to evolve and are meticulously conserved through the eons. Organization is a ?uid medium capable of rapid adaptation. The brain carries organizational ?uidity to the extreme. In its context, typical devices are ion channels, transmitters and receptors, signaling pathways, whole individual neurons or speci?c circuit patterns. The border line between what is to be called device and what a feat of organization is ?owing, given that in time organized s- systems solidify into devices. In spite of the neurosciences' traditional concentration on devices, their aiming point on the horizon must be to understand the principles by which the nervous system ties vast arrays of internal and external variables into one coherent purposeful functional whole - to understand the brain's mechanism of organization. For that purpose a crucial methodology is in silico experimentation. Computer simulation is a convenient tool for testing functional ideas, a sharp weapon for d- tinguishing those that work from those that don't. To be sure, many alternatives can only be decided by direct experiment on the substrate, not by modeling. However, if a functional idea can be debunked as ?awed once tried in silico it would be a waste to make it the subject of a decade of experimentation or discussion. The venture of understanding the function and organization of the visual system illustrates this danger. © 2005 Springer Science+Business Media, Inc. All rights reserved.
C.D. Rollo, C.V. Ko, J.G.A. Tyerman, and L.J. Kajiura Abstract: Sleep is required for the consolidation of memory for complex tasks, and elements of the growth-hormone (GH) axis may regulate sleep. The GH axis also up-regulates protein synthesis, which is required for memory consolidation. Transgenic rat GH mice (TRGHM) express plasma GH at levels 100-300 times normal and sleep 3.4 h longer (30%) than their normal siblings. Consequently, we hypothesized that they might show superior ability to learn a complex task (8-choice radial maze); 47% of the TRGHM learned the task before any normal mice. All 17 TRGHM learned the task, but 33% of the 18 normal mice learned little. TRGHM learned the task significantly faster than normal mice (p < 0.05) and made half as many errors in doing so, even when the normal nonlearners were excluded from the analysis. Whereas normal mice expressed a linear learning curve, TRGHM showed exponentially declining error rates. The contribution of the GH axis to cognition is conspicuously sparse in literature syntheses of knowledge concerning neuroendocrine mechanisms of learning and memory. This paper synthesizes the crucial role of major components of the GH axis in brain functioning into a holistic framework, integrating learning, sleep, free radicals, aging, and neurodegenerative diseases. TRGHM show both enhanced learning in youth and accelerated aging. Thus, they may provide a powerful new probe for use in gaining an understanding of aspects of central nervous system functioning, which is highly relevant to human health.
Sleep is required for the consolidation of memory for complex tasks, and elements of the growth-hormone (GH) axis may regulate sleep. The GH axis also up-regulates protein synthesis, which is required for memory consolidation. Transgenic rat GH mice (TRGHM) express plasma GH at levels 100-300 times normal and sleep 3.4 h longer (30%) than their normal siblings. Consequently, we hypothesized that they might show superior ability to learn a complex task (8-choice radial maze); 47% of the TRGHM learned the task before any normal mice. All 17 TRGHM learned the task, but 33% of the 18 normal mice learned little. TRGHM learned the task significantly faster than normal mice (p < 0.05) and made half as many errors in doing so, even when the normal nonlearners were excluded from the analysis. Whereas normal mice expressed a linear learning curve, TRGHM showed exponentially declining error rates. The contribution of the GH axis to cognition is conspicuously sparse in literature syntheses of knowledge concerning neuroendocrine mechanisms of learning and memory. This paper synthesizes the crucial role of major components of the GH axis in brain functioning into a holistic framework, integrating learning, sleep, free radicals, aging, and neurodegenerative diseases. TRGHM show both enhanced learning in youth and accelerated aging. Thus, they may provide a powerful new probe for use in gaining an understanding of aspects of central nervous system functioning, which is highly relevant to human health.
The target articles on sleep and dreaming are discussed in terms of the concept of search activity integrating different types of behavior, body resistance, REM sleep/dream functions, and the brain catecholamine system. REM sleep may be functionally sufficient or insufficient, depending on the dream scenario, the latter being more important than the physiological manifestation of REM sleep. REM sleep contributes to memory consolidation in the indirect way.
[Nielsen; Revonsuo; Solms; Vertes & Eastman]
The most challenging objections to the Threat Simulation Theory (TST) of the function of dreaming include such issues as whether the competing Random Activation Theory can explain dreaming, whether TST can accommodate the apparently dysfunctional nature of post-traumatic nightmares, whether dreams are too bizarre and disorganized to constitute proper simulations, and whether dream recall is too biased to reveal the true nature of dreams. I show how these and many other objections can be accommodated by TST, and how several lines of new supporting evidence are provided by the commentators. Accordingly TST offers a promising new approach to the function of dreaming, covering a wide range of evidence and theoretically integrating psychological and biological levels of explanation.
The present paper proposes a new psychophysiological approach to the genesis of positive and negative schizophrenic symptoms. According to this approach, the initial factor in schizophrenic disorders is a functional insufficiency of the right hemisphere which can be determined by early emotional experience in combination with subtle brain damage. This functional insufficiency causes (a) the inability to grasp and select information before its realization; and (b) the inability to produce a polysemantic context which is crucial for creativity, psychological defense, and the restoration of search activity, all of which determine psychophysiological adaptation to the environment. Right hemisphere insufficiency causes left hemisphere hyperactivity as an ineffective attempt to compensate for this functional deficiency. As a result, normal search activity is replaced by artificial search activity which is represented by "positive" symptoms, and which uses the predisposition of the left hemisphere's catecholamine system for its increased activity. The suggestion is made that cognitive impairment in schizophrenia (the inability to use appropriate previous information in relation to current perceptual input) is related to the competition between information processing which requires left hemisphere activity, and the formation of positive symptoms, also based on left hemisphere activity.
Two-hour, highly-selective, rest-period, rapid-eye-movement (REM)-sleep deprivation (RD) was performed on rats to characterize the time-course of the homeostatic response to REM-sleep loss. RD caused a dramatic and progressive increase in the frequency of attempts to enter REM sleep, suppressed non-REM sleep EEG delta power, and (in late rest period trials) was followed by a rebound increase in REM-sleep expression.
Rapid eye movement sleep deprivation (REMSD) is a potent stressor in rats. Behavioral abnormalities such as passive and active avoidance, locomotor activity, problem solving, sensory information processing, and the development of adaptive copping strategy in response to repeated stress are among the earliest obvious symptoms of REMSD, the mechanism for which remain largely unknown. The aim of this study was to determine whether 96 h of REMSD causes changes in monoamine neurotransmitters concentrations in rat forebrain regions (frontal cortex, FC; parietal cortex, PC, and striatum) that are involved in mediating higher brain functions such as attentional mechanisms, sensory information processing, and locomotor activity, which are severely affected in REMSD conditions. Rats were subjected to 96 h of REMSD using inverted flower pot water tank technique. To account for the stress associated with water tanks, a tank control group (TC) was included where the animals could reside comfortably on a large pedestal in the water tank. Regional brain concentrations of norepinephrine (NE), dopamine (DA), dihydroxyphenyacetic acid (DOPAC), L-3,4-dihydroxyphenylalanine (L-DOPA), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (HIAA) were determined by electrochemical detection using high-performance liquid chromatography. The concentrations of serotonin and its metabolite, HIAA, was reduced in the frontal and parietal cortexes of REMSD rats compared with TC or cage control (CC) group. NE, DA, DOPAC, and HVA concentrations in FC and PC of REMSD animals were remained unchanged compared with TC or CC rats. A significant increase in the concentrations of DA metabolites was observed in the striatum of REMSD rats when compared with CC and TC rats. There was a 29 and 31% increase in the concentration of striatal DA in REMSD group compared to the TC and CC groups, respectively; however, these percentages were not statistically different. Striatal NE, 5-HT, and HIAA concentrations were not significantly different among the three groups. These results suggest that 96 h of REMSD alters dopaminergic and serotonergic systems in different locations in rat brain. The effect of REMSD on the serotonergic systems are localized in the cerebral cortex, whereas dopaminergic metabolism is increased in the striatum.
Psychoneuroimmunology has become an independent science with a broad experimental basis. However, its theoretical basis is still very vague and ambiguous. There are many contradictions in the experimental data that have not been integrated into a united conception, and some accepted paradigms that remain doubtful. The present critical review suggests a conceptual approach to the problem based on the proposition of two opposite types of behavior (search activity and renunciation of search) with attempts to integrate experimental results by avoiding contradiction. The analysis of the literary data confirms that every behavior that includes search activity prevents psychoimmunological disorders, whereas renunciation of search displays a general predisposition to such disorders. Such an approach makes possible new solutions of paradoxes and broadens the possible interpretations of the alteration of immune functions in depression, anxiety, and stressful events.
Severe brain disorders can be expressed as markedly abnormal encephalopathic EEG patterns in neonates who are usually neurologically depressed, with abnormal levels of reactivity and tone. This symptomatic group is now a minority of medically ill neonates as a result of more vigorous fetal and neonatal resuscitative efforts. Most neonates alternatively express brain dysfunction as more pervasive alterations in EEG-sleep organization or maturation, usually in the absence or after resolution of abnormal clinical signs. One form of dysfunction is expressed as neurophysiologic dysmaturity. Brain dysmaturity may reflect altered rates of development in infants who sustained prenatal or postnatal stresses, as discussed in the first part of this review. We now summarize our findings of dysmature EEG-sleep development at conceptional term ages in an asymptomatic preterm cohort during a prolonged extrauterine period before discharge from the nursery. Dysmaturity of EEG-sleep function was expressed as delayed and/or accelerated physiologic behaviors, as compared with behaviors expected for the conceptional age. Dysmature brain function at conceptional term ages was also associated with poorer neurodevelopmental performances at 12 and 24 months of age. Neuronal pathways which subserve state-specific neurophysiologic behaviors will functionally adapt to stress by either slowing or accelerating neurological maturation. Through ontogenetic brain adaptation, which continues during postnatal development, a balance is maintained between the needs of the present developmental stage and anticipated needs during subsequent stages of maturation. How medical complications and environmental influences interact to promote greater brain dysmaturity in the neonate is still unknown. EEG sleep study can serve as a useful neurophysiologic screening procedure for the child suspected of having a subclinical presentation of an emerging static encephalopathy; longitudinal studies will then document deviations from expected ontogeny in the vulnerable child who is later stressed by environmental and socioeconomic factors.
We studied the influence of a nocturnal environment perceived as warm on the subsequent daytime sleep of healthy human subjects (20–25 years old).
From 00:00 to 8:00, they were kept awake and exposed to either a thermoneutral and comfortable (CN) or a warm and uncomfortable (EW) environment, as assessed by the predicted mean vote/percentage of persons dissatisfied questionnaire (PMV/PPD). The subjects then slept from 8:00 to 14:00 in a thermoneutral environment. Sleep was scored according to the Rechtschaffen and Kales criteria. Rectal temperature was recorded from 22:00 to the end of the sleep period.
Compared to CN, a significant but moderate hyperthermia (0.3–0.4°C) occurred rapidly in EW, and was maintained throughout the night. This modest difference disappeared during subsequent sleep spent at thermal comfort. Exposure to a warm uncomfortable environment before bedtime significantly increased the duration (+37%) and percentage of rapid eye movement sleep (REMS).
This hypnic response could be due to interactions occurring between thermoregulatory, circadian, and sleep mechanisms. It could also be ascribed to synergic actions of the neurophysiological (among others, involving the hypothalamo-pituitary-adrenal axis) and psychological (involving memory processing) processes developed when the organism faces a moderate stress.
The effects of a nocturnal exposure to a cool environment on daytime recovery sleep was studied in eight young (20–25 years old) healthy volunteers. A set of standardized clothing (KSU ensemble type) was provided to each individual (estimated total thermal resistance: 0.6 clo). The subject kept awake was passively exposed from 22.30 to 07.30 hours to environments perceived as neutral (N) and comfortable or slightly cold (C) and uncomfortable. They were then allowed to sleep ad libitum (light out at 08.00 hours) under thermoneutral conditions (air temperature: 21°C to 22°C; clothing: cotton tee-shirt and pajama-pants; covering: one cotton sheet and one wool blanket). Sleep was recorded and scored according to the Rechtchaffen and Kales standard procedures. Esophageal temperature (T
es) was recorded from 21.30 hours until the end of sleep. The nocturnal drops in T
es were significantly different between N and C (p<0.01), this difference disappearing during sleep. No statistical difference was found between conditions for most of the sleep variables. Compared to N however, C resulted in a significant increase in rapid eye movement (REM) sleep duration (+35%, p<0.01) during the subsequent daytime sleep. It is hypothesized that the REM-sleep increase induced by the exposure to moderate cold is due to the thermal discomfort stress consciously perceived by the subject.
The goal of the present paper is to elucidate and to resolve contradictions in the relationships among different forms of stress, sleep deprivation, and paradoxical sleep (PS) functions. Acute immobilization stress and the stress of learned helplessness are accompanied by an increase of PS, whereas the stress of defense behavior and the stress of self-stimulation cause PS reduction. Recovery sleep after total sleep deprivation performed on the rotating platform is marked by a dramatic rebound of PS although NREM (non-rapid eye movement) sleep deprivation is more prominent than PS deprivation. This PS rebound leads to a quick reversal of the pathology caused by prolonged sleep deprivation. The search activity (SA) concept presents an explanation for these contradictions. SA increases body resistance to stress and diseases, whereas renunciation of search (giving up, helplessness) decreases body resistance. PS and dreams contain covert SA, which compensates for the lack of the overt SA in the preceding period of wakefulness. The requirement for PS increases after giving up and decreases after active defense behavior and self-stimulation. Immobilization stress prevents SA in waking behavior and increases the need in PS. Sleep deprivation on the rotating platform, like immobilization stress, prevents SA, produces conditions for learned helplessness and, suppresses PS. Such a combination increases PS pressure and decreases body resistance.
To compare neuropsychological and psychosocial function in children with a history of snoring, children with a history of behavioral sleep problems (BSP), children with both a history of snoring and BSP, and a group of control subjects.
Families awaiting consultation for "sick" visits in 5 general practice clinics completed the Sleep Disturbance Scale for Children. A subset of children were categorized into groups: Snorers (n = 11), BSP (n = 13), Snorers+BSP (n = 9), and controls (n = 31). Children underwent psychological (Wechsler Abbreviated Scale of Intelligence, Children's Memory Scale; Test of Everyday Attention and Auditory Continuous Performance Test) and psychosocial assessment (Child Behavior Checklist).
With analysis of variance, it was revealed that, compared with children in the BSP and control groups, those in the Snorers+BSP and Snorers groups showed reduced intelligence and attention scores. By contrast, compared with children in the Snorers and control groups, children in the Snorers+BSP and BSP groups reported reduced social competency, increased problematic behavior, and reduced memory scores. Children in the combination of Snorers+BSP group showed more deficits than children in all other groups.
In children, snoring and BSP, separately and together, are associated with impaired neuropsychological and psychosocial functioning. Furthermore, snoring and BSP are related to performance in disparate ways. Snoring was associated with intelligence and attention deficits, whereas BSP was associated with memory and behavioral deficits.
Reviews the literature on REM sleep in regard to whether REM sleep prepares the S for subsequent learning or facilitates the retention of learning and/or the adaptation to prior stimulation. It is concluded that when studies are classified paradigmatically, E. M. Dewan's (1969) REM sleep metaprogramming hypothesis provides a useful conceptual scheme for interpreting the relevant literature. Suggested modifications to this hypothesis and anticipated future ones are discussed. (90 ref)
Deprivation of REM sleep (REMD) for about 3 h immediately after each training session greatly impaired brightness discrimination learning in a Y-maze. REMD beginning 2 h after training had no effect. Immediate REMD did not impair position learning in this maze. These results suggested that one function of REM sleep is the consolidation or assimilation of information for which the animal is relatively unprepared, as described by Seligman (1970). Consolidation of learning for which the rat is prepared appears to be independent of REM sleep.
Trained 19 implanted male Walker-Walker rats to barpress for food reward. In a preliminary experiment, a 17½-hr/day partial selective paradoxical sleep (PS) deprivation was alternated with a 6½-hr/rest period. Training was given just before the rest period each day, and EEG and EMG were continuously recorded during the rest periods. PS was observed to increase during task acquisition. These increases were of a prolonged nature, lasting the entire rest period. Extinction training did not appear to alter PS levels. In a more detailed, 24-hr/day continuous recording experiment, the same task was given. No sleep deprivation was imposed, and the Ss were normally rested. Both PS and slow-wave sleep were found to be increased during the training sessions. Possible relationships between these sleep parameter changes and learning are discussed. (25 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
That all events are equally associable and obey common laws is a central assumption of general process learning theory. A continuum of preparedness is defined which holds that organisms are prepared to associate certain events, unprepared for some, and contraprepared for others. A review of data from the traditional learning paradigms shows that the assumption of equivalent associability is false. Examples from experiments in classical conditioning, instrumental training, discrimination training, and avoidance training support the assumption. Language acquisition and the functional autonomy of motives are also viewed using the preparedness continuum. It is speculated that the laws of learning themselves may vary with the preparedness of the organism for the association and that different physiological and cognitive mechanisms may covary with the dimension. (2 p. ref.) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Eighty-eight adult white rats were divided into 9 groups. Groups 1 and 2 served as controls. The rats of Group 3 were repeatedly aroused during 4 days at the very onset of each REM-sleep period by direct midbrain reticular formation stimulation. This deprivation decreased the daily amount of REM-sleep by 70%, while slow-wave sleep was reduced by 10% only. In Group 4, the animals were given food and water for 1 h a day only. Groups 5 and 6 were subjected to immobilization and cold stress, respectively. Groups 7, 8 and 9 were deprived of REM-sleep on platforms of 15, 11 and 6.5 cm in diameter, respectively. Stress was estimated by the classical Selye's triad: weight of adrenals and thymus and gastric ulceration. Emotionality was measured in the open-field and also by self-stimulation of the lateral hypothalamus. Neither emotional behavior disturbances nor Selye's stress features were found after REM-deprivation in Group 3. Moreover, arousal deprivation induced a slight, though significant, reduction in adrenal weight. Also, no changes in emotional behavior were noted in stress-exposed groups (5 and 6). Only the interplay between REM-sleep deprivation and stress on the platforms (Groups 7, 8 and especially 9) led to a considerable shift in emotionality.
When an individual shows emotional behavior he or she very often is in a state of high physiological activation. However, sometimes apparently emotional behavior (aggression, fear) may be associated with moderate or even low levels of activation. This chapter deals with the psychological mechanisms that determine this internal state. Whenever an organism faces a threat, the brain responds with a generalized and fairly standard “program,” which is referred to as activation in this chapter. In addition, one or several specific response patterns is chosen and “executed” by the brain, and these are referred to as emotional programs. Even if such programs occur together in many instances, they are regarded as due to independent mechanisms localized in separate parts of the brain. There seems to be an interaction between these specific programs and the internal state, and this interaction is the main topic of this chapter. The main assumption is that instrumental behavior reduces the activation level, and that emotional programs do not differ in principle from other types of behavior in their instrumental effects on the environment and the internal state.
The effect of sleep deprivation on working memory for spatial information was evaluated. Rats were trained on a win-shift strategy in an eight-arm maze until they exhibited accurate retention when an 8-h delay was imposed between the fourth and fifth choices. Then the effects on spatial memory of depriving the rats of sleep throughout the retention interval were compared with the influence of a stress control (swimming for 1 h during the retention interval) or no treatment, using a counterbalanced within-subjects design. Although sleep deprivation produced a marginally significant impairment in spatial memory at a 4-h delay, in two replications at an 8-h delay interval there was no suggestion of an effect of sleep deprivation. Thus, spatial memory in the radial maze remains intact after brief periods of sleep deprivation. The present findings are consistent with other recent studies, all of which demonstrate the remarkable resistance to disruption by retroactive treatments of the rat’s spatial memory system.
EEG and EMG recordings were taken at the same time each day over a 3-h period, and the duration of paradoxical and slow wave sleep noted for each day. After several days, experimental groups underwent two-way shuttlebox avoidance conditioning prior to the daily recording session. Trials were either crowded (70 trials in a single session) or distributed (one 15-trial session each day); in the latter condition, the learning sessions were continued for each rat until asymptote performance was reached. Control groups were tested for the effects of shock and tone stimulation.The control rats showed no significant change in PS duration at any time during the experiment. In the experimental groups there was, by contrast, a significant increase in PS and, in the distributed condition, this increase was related to the degree of learning achieved, but on the fourth day, when performance reached the asymptote PS duration returned to the reference level. The increased duration of PS in the experimental groups was due to an increase in the number of PS phases, the average duration of each phase not showing any change. It should be added that the increases were found only in the first half-hour of sleep; the effect would thus appear to be immediate and short-lasting.
Animal studies relating REM sleep to information processing were reviewed. With several tasks, increased REM sleep following training was found in rats and cats. Deprivation of REM sleep after training in these situations impaired retention. Deprivation of REM sleep before training impaired assimilation of new information in rats and mice, perhaps by altering neurochemical factors involved in modulation of the memory trace. Some species differences among rats, cats and mice in the involvement of REM sleep in information processing were discussed. Finally, the relation of information processing to other hypothetical functions of REM sleep was considered.
Effects of instrumental and pharmacological deprivation of sleep on Y-maze learning have been studied in two inbred strains of mice (C57BR/cd/Orl and C57BL/6/Orl), having identical sleep rhythms, but mainly differing in their ability to learn.Administration of α-methyl-DOPA (100 mg/kg) provokes complete suppression of paradoxical sleep (PS) for 9–11 h.Injection immediately after each training session over the first 5 days caused a delay in acquisition of an active avoidance task in C57BR mice. Treated C57BL/6 mice exhibited a significant facilitation of acquisition. Similar results were obtained by instrumental deprivation of sleep for 10 h.AbstractLes effets de la privation instrumentale et pharmacologique du sommeil ontétéétudiés sur l'apprentissage d'un labyrinthe en Y chez 300 souris consanguines C57BR/cd/Orl et C57BL/6/Orl. Ces deux souches présentent la meˆme organisation temporelle au sommeil (durée, rythme), mais diffèrent par leur vitesse d'acquisition d'un conditionnement complexe.L'α-méthyl-DOPA (100 mg/kg) supprime complètement le sommeil paradoxal (SP) pendant 9–11 h. Injectée immédiatement après chaque séance de conditionnement, cette substance provoque un retard d'acquisition de l'évitement actif chez les souris C57BR par rapport aux témoins recevant le solvant. Dans les meˆmes conditions expérimentales, on observe au contraire chez les souris C57BL/6 une facilitation significative du conditionnement.Des résultats similaires ontétéobtenus après privation instrumentale de sommeil pendant 10 h.
During avoidance conditioning in the Cat, arousal, heart rate and respiratory reactions produced by the conditioned stimulus (CS) were recorded. The development of these reactions was compared with the paradoxical sleep (PS) length measured between the trials of each experimental session. The results of this analysis point to the existence of a critical learning period characterised by a high rate of central and peripheral reactions and by an increase in PS length. This period precedes the stabilization of performances. The functional relationship of these two phenomena with each other and with learning is discussed.
We hypothesize that rapid eye movements (REM) sleep may play a role in maintaining the functioning of catecholamine-containing neurons in the central nervous system. The main lines of evidence supporting this view are (a) following REM deprivation the responsiveness of catecholamine systems is depressed; (b) administration of drugs which enhance catecholamine activity can reverse some of the behavioral deficits which occur after REM deprivation; and (c) acute administration of pharmacological agents which depress catecholamine activity (alpha methyltyrosine, reserpine) produce a “compensatory≓ increase in REM time whereas increasing central catecholamine availability at the synapse (electroconvulsive shock, imipramine, monoamine oxidase inhibitors) decreases REM sleep. It is suggested that the mechanism of REM is primarily cholinergic and that the locus coeruleus may be the site of interaction between the catecholamine-REM function and the cholinergic-REM mechanism. Evidence is discussed relating to the possibility that REM sleep may have a more general function in the central nervous system, i.e., the modulation of protein synthesis in the brain.
Four days of desynchronized sleep (D) deprivation (island technique) produced a significant deficit in subsequent acquisition of an active avoidance task in the rat. Four days of repeated stress resulting in similar adrenal and thymus changes had no effect on acquisition. L-dopa 200 mg/kg in normals produced a significant deficit in acquisition, but L-dopa after four days of D-deprivation resulted in normal acquisition. (Thus L-dopa reversed the learning deficits produced by D-deprivation, an effect we have shown previously for MAO inhibitors and imipramine.) Alpha-methylparatyrosine also produced a deficit in avoidance acquisition, and L-dopa significantly reduced this deficit, suggesting that the catecholamine increase produced by L-dopa is involved. We suggest that D-deprivation produces defects in the functioning of central catecholaminergic neuronal systems, and that the defects are reversible by increasing the availability of catecholamines.
The fact that sleep is associated with very active endogenous neural (chemical and electrical) processes, suggests that these processes may be involved in the maintenance of long-term memory storage. The present experiments were designed to examine the hypothesis that rapid eye movement (REM) sleep deprivation will produce impairment of long-term memory. Mice deprived of REM sleep for 3, 5 or 7 continuous days, during the interval between a one-trial inhibitory avoidance training experience and a subsequent retention test, displayed a temporary retrograde amnesia when tested 30 min or three hr following termination of REM deprivation. The mice did not recover from the amnesia if electroconvulsive shock was administered immediately following the interval of REM sleep deprivation. In a further study, the generality of these findings was obtained by depriving mice of REM sleep during the interval between a discrimination training experiment in a black-white T-maze and the subsequent retention test.
Pairs of rats were placed in an apparatus where their sole food source hung over an electrified grid. The current was shut off only while one rat remained on a platform out of reach of the food, thus allowing his partner to eat. Mastery of the process of taking turns at eating required about 10 daily sessions. Injection of imipramine or chlordiazepoxide a few minutes after each feeding session prevented the development of this cooperative behavior. Drug injection 3 hrs after each session had no effect. Suppression of REM sleep during the first 3 hrs after training was considered the most likely mechanism of the drug-induced impairment.
Effects of instrumental and pharmacological deprivation of sleep on Y-maze learning have been studied in two inbred strains of mice (C57BR/cd/Orl and C57BL/6/Orl), having identical sleep rhythms, but mainly differing in their ability to learn. Administration of alpha-methyl-DOPA (100 mg/kg) provokes complete suppression of paradoxical sleep (PS) for 9-11 h. Injection immediately after each training session over the first 5 days caused a delay in acquisition of an active avoidance task in C57BR mice. Treated C57BL/6 mice exhibited a significant facilitation of acquisition. Similar results were obtained by instrumental deprivation of sleep for 10 h.
Reviews the literature on REM sleep in regard to whether REM sleep prepares the S for subsequent learning or facilitates the retention of learning and/or the adaptation to prior stimulation. It is concluded that when studies are classified paradigmatically, E. M. Dewan's (1969) REM sleep metaprogramming hypothesis provides a useful conceptual scheme for interpreting the relevant literature. Suggested modifications to this hypothesis and anticipated future ones are discussed. (90 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Basing themselves on an analysis of data cited by other researchers and the results of their own investigation, conducted on man and animals, the authors disclose that sleep changes are determined by the type of behavioural reaction to emotional stress: the behaviour that includes components of search activity directed at changing the situation is accompanied by a reduction of REM sleep time; renunciation of search, as in the cases of passive avoidance, neurotic anxiety and depression, is attended by an increase in REM sleep requirement. Presumably, the function of REM sleep is to compensate for renunciation of search in the waking period. The authors suggest a method of appraising the character of reaction to stress by sleep changes--calculation of the time ratio of REM sleep to delta-sleep in the first two cycles.
Animal studies are examined in relation to the sleep-learning hypothesis. It is concluded that the data best support the idea of special periods of paradoxical sleep (PS) within the 24 hour period which are specifically involved with the learning process. The onset and duration of these PS "windows" varies with strain of animal, type of task and number of training trials per session. Alternative explanations and theories are considered.
Rats were deprived of rapid eye movement (REM) sleep for up to five days by confinement to a small platform surrounded by water. Acquisition of three tasks—passive avoidance, active avoidance, and an appetitive alternation discrimination—was slower following REM sleep deprivation than after normal (home cage) or stress control (immersed in cold water) treatments. Sleep loss controls, who had reduced non-REM sleep, performed as well as normals and better than the REM sleep deprived rats on the two shock avoidance tasks—the alternation test was not employed. Thus, five days of REM sleep deprivation in the rat produced marked acquisition deficits which were not task specific and which did not appear to be due to nonspecific stress, non-REM sleep loss, or changes in activity levels.
To determine the effects of deprivation of rapid eye movement (REM) sleep on the behavior and maze learning ability of rats, 51 male albinos were trained in a T maze and each was assigned to one of four groups matched on learning ability. Three of the four groups were then placed on small water-surrounded platforms and subjected to one of the following conditions for 26 days: Groups SPE and SPC were confined to small platforms and thus deprived of REM sleep, while group LPC was positioned on larger platforms. The subjects in the fourth group were home cage controls. The platform animals were removed to their home cages for three hours each day where only the SPE animals were kept in a wakeful state. During the deprivation period, each of the animals were paired daily with a member of his own or another group in a neutral cage and rated for aggression.At the conclusion of the deprivation period, five animals from each group were sacrificed and the brain removed for pathological examination. The remaining animals were tested for retention and reversal in the T maze and then began an acquisition series in Lashley's Maze III.Results indicated that the animals maze learning ability was not consistently affected by the deprivation procedure and no neuropathology was observed. Deprivation resulted in a significant increase in aggressive behavior, however. It was hypothesized that the central nervous system of most animals is capable of tolerating prolonged REM sleep deprivation, carrying on during wakefulness those processes normally subserved by the REM phase.
The purpose of this study was to determine if a correlation existed between paradoxical sleep and learning capabilities in mice. The hypothesis would predict that the best learners would have the highest percentage of paradoxical sleep. Seven different inbred strains of mice and random-bred Swiss, the types used by Bovet in his learning studies, were implanted with cortical electrodes and their sleep studied electroencephalographically. A significant positive correlation was found between the amount of paradoxical sleep and learning ability on active avoidance tasks for the strains studied.
Two strains of mice were subjected to a complex shock avoidance task. The C57BR (brown) strain were superior to the C57BL (black) strain in their learning ability. Both strains showed a long term increase in paradoxical sleep (PS) prior to the maximum increase in learning performance (MIP). For the brown starin, this increase was apparent in the 24 h before the MIP. For the black strain, the increase began 48 h prior to the MIP. In the brown strain the day after the MIP, a second effect appeared. PS was higher in the first half hour after sleep onset, following the training session. This increase was due to the larger numbers of slow wave sleep-paradoxical sleep (SWS-PS) cycles. The effect was not present in the black strain.It was concluded that two mechanisms are probably at work during the learning process, one during the earlier stages and one during the later stages as learning reaches criterion.
The authors tried to demonstrate how, in species having rapid eye movement (REM) sleep, this mechanism plays a role in adaptation to external events. The development of this mechanism appears in species that show increasing abilities to assimilate unusual information into the nervous system. The authors suggest that the evolutionary development of this neurophysiologic mechanism has made possible the increasing flexible use of information in the mammalian family. That this process occurs during sleep seems to fit with current thinking about programming and reprogramming of information processing systems. Thus, several authors have pointed out the advantage of a separate mechanism for reprogramming the brain in order to avoid interference with ongoing functions. This formulation of a function for REM sleep suggests that future studies should attempt to characterize the various kinds of information processing which are served by this mechanism in the differing species which exhibit it.
This experiment provides evidence that learning induces a protracted augmentation of paradoxical sleep (PS) time, lasting for at least 24 h.Albino mice are studied in a counterbalanced crossover design experiment in which each animal is used as its own baseline control and yoke control. The animals are trained for 1 h in an active avoidance task in which the experimental subjects learn to avoid shock as compared to yoke controls receiving an equal number of shocks, but are unable to escape.The statistical analyses reveal that slow wave sleep (SWS) is augmented in the experimental and yoke control subjects, whereas PS isonly augmented in the experimentals. The analyses also reveal that the PS augmentation is primarily a function of a specific increase of the number of PS periods, without any change in the average duration of each PS phase. Further analyses between a slow learning group of animals and fast learners indicate that the PS augmentation is most marked in the slow learners. The results suggest that SWS augmentation is related to the CS-footshock contingency, whereas PS augmentation is a function of something quite unique about a mouse learning to escape or avoid a footshock.This study, taken together with our previous work, suggests that PS augmentation may be a neurobiological expression of the long-term process of memory consolidation.
The author discusses a number of controversial aspects of the search activity concept. This concept, based on an analysis of data cited by other researchers and the results of the author's own investigation, performed together with V. V. Arshavsky, postulates that search activity raises the body's resistance to stress and experimentally induced pathology whereas renunciation of search forms a nonspecific predisposition to somatic disturbances (e.g., psychosomatic disease). REM sleep is regarded as a specific form of search activity aimed at compensating for the state of renunciation of search in walking. In this paper the author argues that 1) renunciation of search can be accompanied either by anxiety or by depression, 2) REM sleep deprivation on a "small platform" raises the requirement in REM sleep by producing renunciation of search, 3) during search activity brain catecholamine synthesis is stimulated by catabolism whereas a state of renunciation of search upsets this feedback system. The actuation of the brain mechanisms of search in REM sleep necessitates a certain brain catecholamine level. If the brain catecholamine level is very high during waking behavior due to intensive search activity, the REM sleep requirement is low, REM sleep becoming reduced. After a moderate drop in the brain catecholamine level at the initial stage of renunciation of search the requirement in REM sleep rises and this phase grows longer. But at the late stage of renunciation of search the brain catecholamine level drops extremely, REM sleep shrinking in spite of the great appropriate requirement, and 4) the functional insufficiency of REM sleep invites various forms of pathology.
In order to examine the hypothesis that active (REM) sleep contributes to the enhanced brain development which is observed in rats reared under enriched conditions, 3 groups of female rats were assigned at 28 days after birth to either: (a) daily 2.5 h exposure to an enriched environment, followed immediately by active sleep deprivation (clonidine injection); (b) daily environmental enrichment plus vehicle only; or (c) daily vehicle injection, but continuous rearing under standard laboratory conditions. In addition, so as to control for a possible direct pharmacological effect upon cortical growth, another series of rats was chronically injected with clonidine or saline under standard conditions. At 65 days of age all the animals were sacrificed and the brains dissected into different regions for weighing. A significant increase in total brain weight (mainly due to a heavier cerebral cortex) was found in the enriched-saline group as compared with the standard-saline controls. In contrast, the enriched-clonidine rats showed no differences from the standard-saline group. Moreover, no significant differences were found between clonidine- and saline-injected rats reared in the standard environment. The results indicate that active sleep and central NA activity play a role in growth-promoting effects of environmental stimulation upon specific brain regions.
The issue of whether sleep is physiologically necessary has been unresolved because experiments that reported deleterious effects of sleep deprivation did not control for the stimuli used to prevent sleep. In this experiment, however, experimental and control rats received the same relatively mild physical stimuli, but stimulus presentations were timed to reduce sleep severely in experimental rats but not in controls. Experimental rats suffered severe pathology and death; control rats did not.
Search activity and adapta-tion. Moscow: Nauka
- V S Rotenberg
- V V Arshavsky
Rotenberg, V. S.; Arshavsky, V. V. Search activity and adapta-tion. Moscow: Nauka; 1984.
On depression, development and death
- M E P Seligman
- Helplessness
Seligman, M. E. P. Helplessness. On depression, development and death. San Francisco: Freeman; 1975.
Paradoxical sleep-protection from stress? Sci
- V S Rotenberg
- V V Kovalzon
- V L Tsibulsky
Rotenberg, V. S.; Kovalzon, V. V.; Tsibulsky, V. L. Paradoxical sleep-protection from stress? Sci. USSR 2:45-51; 1986.
The role of memory in rats
- D A Gorelick
- T R Bozewicz
- W H Bridger
Gorelick, D. A.; Bozewicz, T. R.; Bridger, W. H. The role of memory in rats. Bull. Psychol. Soc. 16:408-409; 1980. catecholamines in animal learning and memory. In: Friedhof, A.
Cutting the REM nerve: An ap-proach to the adaptive role of REM sleep Desinchronized sleep deprivation: Learning deficit and its reversal by increased catecholamines
- R Greenberg
- C Pearlman
Greenberg, R.; Pearlman, C. Cutting the REM nerve: An ap-proach to the adaptive role of REM sleep. Perspect. Biol. Med. 17:513-521; 1974. I0. Hartmann, E.; Stern, W. C. Desinchronized sleep deprivation: Learning deficit and its reversal by increased catecholamines. Physiol. Behav. 8:585-587; 1972.
REM sleep, stress and search activity
- Rotenberg
Sleep states and learning. A review of the animal literature
- Smith