Development of REM and slow wave sleep in the rat

1997 ◽  
Vol 272 (6) ◽  
pp. R1792-R1799 ◽  
Author(s):  
M. G. Frank ◽  
H. C. Heller
Keyword(s):  
Slow Wave ◽  
Rem Sleep ◽  
Maternal Separation ◽  
Slow Wave Sleep ◽  
Transient State ◽  
Quiet Sleep ◽  
Immature Form ◽  
The Relationship ◽  
Developing Rat

Active sleep (AS) in the neonate has been considered to be an immature form of rapid eye movement (REM) sleep. Quiet sleep (QS) has been thought to represent an immature form of slow wave sleep (SWS). To determine the relationship between the behaviorally determined states of AS and QS and electrographically determined REM sleep and SWS, we examined sleep ontogeny in the developing rat using an experimental routine that permitted long-term recordings and minimized the effects of maternal separation. Under these conditions, a transient state that included electroencephalographic slow wave activity and phasic motor activity was eventually replaced with the mature SWS pattern. Our work suggests that neonatal QS is not an immature form of SWS and that AS is best considered as an undifferentiated behavioral state from which both SWS and REM sleep develop.

scholarly journals Enhanced Slow Wave Sleep in Patients with Prolactinoma

1998 ◽  
Vol 83 (8) ◽  
pp. 2706-2710 ◽  
Author(s):  
Ralf-Michael Frieboes ◽  
Harald Murck ◽  
Günter Karl Stalla ◽  
Irina A. Antonijevic ◽  
Axel Steiger
Keyword(s):  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Sleep Regulation ◽  
Endocrine Diseases ◽  
Term Administration ◽  
Secondary Hypogonadism ◽  
Bidirectional Interactions

abstract Bidirectional interactions between nocturnal hormone secretion and sleep regulation are well established. In particular, a link between PRL and rapid eye movement (REM) sleep has been hypothesized. Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep. Furthermore, sleep disorders are frequent symptoms in patients with endocrine diseases. We compared the sleep electroencephalogram of seven drug-free patients with prolactinoma (mean PRL levels 1450 ± 1810 ng/mL; range between 146 and 5106 ng/mL) with that of matched controls. The patients had secondary hypogonadism but no other endocrine abnormalities. They spent more time in slow wave sleep than the controls (79.4 ± 54.4 min in patients vs. 36.6 ± 23.5 min in controls, P < 0.05). REM sleep variables did not differ between the samples. Our data suggest that chronic excessive enhancement of PRL levels exerts influences on the sleep electroencephalogram in humans. Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL. These findings are in accordance with reports of good sleep quality in patients with prolactinoma, which is in contrast to that of patients with other endocrine diseases.

Effects of temperature on sleep in the developing rat

1998 ◽  
Vol 274 (4) ◽  
pp. R1087-R1093
Author(s):  
Roger N. Morrissette ◽  
H. Craig Heller
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
State Structure ◽  
Rat Pups ◽  
The Relationship ◽  
Developing Rat ◽  
Wake State

In altricial species, such as humans and rats, much of the development of autonomic systems occurs postnatally. Consequently, vulnerabilities exist early in postnatal development when immature autonomic functions are challenged by external factors such as variations in ambient temperature (Ta). Ta profoundly influences sleep/wake state structure in adult animals and humans, and exposure to excessive warmth has been implicated as a risk factor in sudden infant death syndrome. To better understand the relationship between temperature and sleep during development, we investigated the effect of Ta variation on sleep/wake state structure and sleep intensity in developing rats. In this experiment, sleep intensity was measured by the intensity of slow-wave activity during slow-wave sleep. Neonatal Long-Evans hooded rat pups were surgically prepared for chronic sleep/wake state and brain temperature (Tbr) recording. Two-hour recordings of sleep/wake state and Tbr were obtained from rats on postnatal day 12( P12), P14, P16, P18, and P20 at a Ta of either 28.0–30.0, 33.0–35.0, or 38.0–40.0°C. Ta significantly influenced sleep/wake state structure but had little, if any, effect on sleep intensity in developing rats.

Neostriatal administration of somatostatin: differential effect of small and large doses on behavior and motor control

1977 ◽  
Vol 55 (2) ◽  
pp. 234-242 ◽  
Author(s):  
M. Rezek ◽  
V. Havlicek ◽  
L. Leybin ◽  
C. Pinsky ◽  
E. A. Kroeger ◽  
...  
Keyword(s):  
Motor Control ◽  
Eye Movements ◽  
Slow Wave ◽  
Rem Sleep ◽  
Differential Effect ◽  
Slow Wave Sleep ◽  
Small Doses ◽  
Freely Moving ◽  
Behavioral Excitation ◽  
Higher Doses

The administration of small doses of somatostatin (SRIF) (0.01 and 0.1 μg) into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS). In contrast, the higher doses of SRIF (1.0 and 10.0 μg) caused movements to be uncoordinated and frequently induced more severe difficulties in motor control such as contralateral hemiplegia-in-extension which restricted or completely prevented the expression of normal behavioral patterns. As a result, the animals appeared drowsy and inhibited. Analysis of the sleep-waking cycle revealed prolonged periods of a shallow SWS while REM sleep and deep SWS were markedly reduced; electroencephalogram recordings revealed periods of dissociation from behavior. The administration of endocrinologically inactive as well as the active analogues of SRIF failed to induce effects comparable with those observed after the administration of the same dose of the native hormone (10.0 μg).

scholarly journals Insights into paradoxical (REM) sleep homeostatic regulation in mice using an innovative automated sleep deprivation method

SLEEP ◽  
2020 ◽  
Vol 43 (7) ◽  
Author(s):  
Sébastien Arthaud ◽  
Paul-Antoine Libourel ◽  
Pierre-Hervé Luppi ◽  
Christelle Peyron
Keyword(s):  
Slow Wave ◽  
Rem Sleep ◽  
High Efficiency ◽  
Environmental Changes ◽  
Slow Wave Sleep ◽  
Paradoxical Sleep ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Homeostatic Regulation ◽  
External Modulation

Abstract Identifying the precise neuronal networks activated during paradoxical sleep (PS, also called REM sleep) has been a challenge since its discovery. Similarly, our understanding of the homeostatic mechanisms regulating PS, whether through external modulation by circadian and ultradian drives or via intrinsic homeostatic regulation, is still limited, largely due to interfering factors rendering the investigation difficult. Indeed, none of the studies published so far were able to manipulate PS without significantly altering slow-wave sleep and/or stress level, thus introducing a potential bias in the analyses. With the aim of achieving a better understanding of PS homeostasis, we developed a new method based on automated scoring of vigilance states—using electroencephalogram and electromyogram features—and which involves closed-loop PS deprivation through the induction of cage floor movements when PS is detected. Vigilance states were analyzed during 6 and 48 h of PS deprivation as well as their following recovery periods. Using this new automated methodology, we were able to deprive mice of PS with high efficiency and specificity, for short or longer periods of time, observing no sign of stress (as evaluated by plasma corticosterone level and sleep latency) and requiring no human intervention or environmental changes. We show here that PS can be homeostatically modulated and regulated while no significant changes are induced on slow-wave sleep and wakefulness, with a PS rebound duration depending on the amount of prior PS deficit. We also show that PS interval duration is not correlated with prior PS episode duration in the context of recovery from PS deprivation.

Each distinct type of mental state is supported by specific brain functions

2000 ◽  
Vol 23 (6) ◽  
pp. 941-943 ◽  
Author(s):  
Claude Gottesmann
Keyword(s):  
Slow Wave ◽  
Mental State ◽  
Rem Sleep ◽  
Psychological Functioning ◽  
Slow Wave Sleep ◽  
Mental Content ◽  
Distinct Type ◽  
Inhibitory Processes ◽  
Brain Functions

Reflective waking mentation is supported by cortical activating and inhibitory processes. The thought-like mental content of slow wave sleep appears with lower levels of both kinds of influence. During REM sleep, the equation: activation + disinhibition + dopamine may explain the often psychotic-like mode of psychological functioning.[Hobson et al.; Nielsen; Revonsuo; Solms; Vertes & Eastman]

scholarly journals Slow Wave Sleep and REM Sleep Awakenings Do Not Affect Sleep Dependent Memory Consolidation

SLEEP ◽  
2009 ◽  
Vol 32 (3) ◽  
pp. 302-310 ◽  
Author(s):  
Lisa Genzel ◽  
Martin Dresler ◽  
Renate Wehrle ◽  
Michael Grözinger ◽  
Axel Steiger
Keyword(s):  
Slow Wave ◽  
Rem Sleep ◽  
Memory Consolidation ◽  
Slow Wave Sleep

scholarly journals 0084 Sleep Consolidates Incidentally Encoded Information After Deep but Not Shallow Encoding

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A34-A34
Author(s):  
E M Wernette ◽  
K M Fenn
Keyword(s):  
Slow Wave ◽  
Memory Consolidation ◽  
Slow Wave Sleep ◽  
Declarative Memory ◽  
Memory Performance ◽  
Memory Test ◽  
Memory Traces ◽  
Incidental Encoding ◽  
The Relationship ◽  
With Memory

Abstract Introduction Slow wave sleep (SWS) strengthens declarative memory for information studied for a later test. However, research on the effect of sleep on information that is not intentionally remembered is scare. Previous research from our lab suggests sleep consolidates some, but not all, information that has been encoded incidentally, meaning that it has been acted on but not intentionally remembered. It remains unclear what determines which information benefits from sleep-dependent consolidation processes and what aspects of sleep are related to these mnemonic benefits. In two experiments, we test the hypothesis that sleep consolidates strong but not weak memory traces following incidental encoding, and assess the relationship between memory performance and objective sleep characteristics. Methods In Experiment 1, participants rated words one (weak traces) or three times (strong traces) in a deep or shallow incidental encoding task. Participants either rated words on a scale from ‘concrete’ to ‘abstract’ (deep) or counted the vowels in the words (shallow). Following a 12-hour period containing sleep or wakefulness, participants took a surprise memory test. In Experiment 2, participants rated words one or three times in the deep encoding task, received an 8-hour sleep opportunity with polysomnography, and took the surprise memory test. Results In Experiment 1, participants remembered words better after sleep than wake regardless of whether words were encoded one or three times, but only after deep encoding. Sleep did not consolidate information following shallow encoding. Experiment 2 is ongoing, but we predict that the amount of SWS will correlate positively with memory. Conclusion Results thus far suggest sleep may have consolidated information based on the strength of memory traces. Because deep encoding results in stronger memory traces than shallow encoding, this work is broadly consistent with theories of memory consolidation that predict sleep is more beneficial for strong memory traces than weak, such as the synaptic downscaling hypothesis. Support N/A

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