The two stages of slow wave sleep in the cat and their relation to REM sleep

1968 ◽  
Vol 11 (2) ◽  
pp. 347-356 ◽  
Author(s):  
Reidun Ursin
1977 ◽  
Vol 55 (2) ◽  
pp. 234-242 ◽  
Author(s):  
M. Rezek ◽  
V. Havlicek ◽  
L. Leybin ◽  
C. Pinsky ◽  
E. A. Kroeger ◽  
...  

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).


SLEEP ◽  
2020 ◽  
Vol 43 (7) ◽  
Author(s):  
Sébastien Arthaud ◽  
Paul-Antoine Libourel ◽  
Pierre-Hervé Luppi ◽  
Christelle Peyron

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.


2000 ◽  
Vol 23 (6) ◽  
pp. 941-943 ◽  
Author(s):  
Claude Gottesmann

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]


SLEEP ◽  
2009 ◽  
Vol 32 (3) ◽  
pp. 302-310 ◽  
Author(s):  
Lisa Genzel ◽  
Martin Dresler ◽  
Renate Wehrle ◽  
Michael Grözinger ◽  
Axel Steiger

2013 ◽  
Vol 36 (6) ◽  
pp. 610-611 ◽  
Author(s):  
Sen Cheng ◽  
Markus Werning

AbstractWe propose that rapid eye movement (REM) and slow-wave sleep contribute differently to the formation of episodic memories. REM sleep is important for building up invariant object representations that eventually recur to gamma-band oscillations in the neocortex. In contrast, slow-wave sleep is more directly involved in the consolidation of episodic memories through replay of sequential neural activity in hippocampal place cells.


2010 ◽  
Vol 104 (4) ◽  
pp. 2194-2202 ◽  
Author(s):  
Philip H. de Guzman ◽  
Farhang Nazer ◽  
Clayton T. Dickson

Non-REM (slow-wave) sleep has been shown to facilitate temporal lobe epileptiform events, whereas REM sleep seems more restrictive. This state-dependent modulation may be the result of the enhancement of excitatory synaptic transmission and/or the degree of network synchronization expressed within the hippocampus of the temporal lobe. The slow oscillation (SO), a ∼1 Hz oscillatory pattern expressed during non-REM sleep and urethane anesthesia, has been recently shown to facilitate the generation, maintenance, and propagation of stimulus-evoked epileptiform activity in the hippocampus. To further address the state-dependent modulation of epileptic activity during the SO, we studied the properties of short-duration interictal-like activity generated by focal application of penicillin in the hippocampus of urethane-anesthetized rats. Epileptiform spikes were larger but only slightly more prevalent during the SO as opposed to the theta (REM-like) state. More notably, however, epileptic spikes had a significant tendency to occur just following the peak negativity of ongoing SO cycles. Because of the known phase-dependent changes in 1) synaptic excitability (just following the positive peak of the SO) and 2) network synchronization (during the negative peak of the SO), these results suggest that it is the synchrony and not the changes in synaptic excitability that lead to the facilitation of epileptiform activity during sleep-like slow wave states.


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