Enhancement of slow-wave sleep by endotoxin and lipid A

1986 ◽  
Vol 251 (3) ◽  
pp. R591-R597 ◽  
Author(s):  
J. M. Krueger ◽  
S. Kubillus ◽  
S. Shoham ◽  
D. Davenne
Keyword(s):  
Cell Wall ◽  
Slow Wave ◽  
Lipid A ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Dose Range ◽  
State Transitions ◽  
Sleep State ◽  
Cell Wall Component ◽  
Bacterial Peptidoglycan

Some muramyl peptides derived from bacterial peptidoglycan enhance slow-wave sleep (SWS). The purpose of this study was to test whether another cell wall component, lipopolysaccharide (LPS), and its lipid A moiety also have an effect on sleep. When injected intravenously, both LPS and lipid A enhanced the duration of SWS, increased electroencephalogram delta-wave amplitudes, suppressed rapid eye movement (REM) sleep, and induced biphasic fevers. The effects of intravenously administered lipid A and LPS on SWS were present primarily during the first 3 h postinjection. Intraventricular lipid A administration enhanced SWS, did not suppress REM, and induced a monophasic fever; the SWS effect had a 3-h latency, whereas temperature started to rise during the second hour. Regardless of the route of administration, within the dose range used here, sleep was normal by the following criteria: sleep was episodic, animals could be easily aroused, and brain temperature, although elevated to "febrile" levels, continued to fluctuate during sleep-state transitions indistinguishably from control conditions. We conclude that LPS and lipid A are capable of modulating sleep.

Waking and ventilatory responses to laryngeal stimulation in sleeping dogs

1978 ◽  
Vol 45 (5) ◽  
pp. 681-689 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson
Keyword(s):  
Endotracheal Tube ◽  
Eye Movement ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Sleep State ◽  
Ventilatory Responses ◽  
Cardiac Responses ◽  
Prolonged Apnea ◽  
Sleep Arousal

We studied waking and ventilatory responses to laryngeal stimulation during sleep in three dogs. The dogs breathed through an endotracheal tube inserted caudally into the trachea through a tracheostomy. Laryngeal stimulation was produced either by inflating a small balloon that was positioned in the rostral tracheal segment, or by squirting water onto the larynx through a catheter inserted through the tracheostomy. Airflow was measured with a pneumotachograph, and sleep state was determined by behavioral, electroencephalographic, and electromyographic criteria. We found that the degree of laryngeal stimulation required to produce arousal and coughing was higher in rapid-eye-movement (REM) sleep than in slow-wave sleep (SWS). Stimuli that failed to cause arousal from SWS often produced a single expiratory effort, or brief apnea (1--2 s) and bradycardia. In contrast, during REM sleep subarousal stimuli often resulted in prolonged apnea (greater than 10 s) and marked bradycardia. We conclude that during REM sleep arousal responses to laryngeal stimulation are depressed, but ventilatory and cardiac responses are intact.

Brain temperature changes coupled to sleep states persist during interleukin 1-enhanced sleep

1986 ◽  
Vol 250 (1) ◽  
pp. R96-R103 ◽  
Author(s):  
J. Walter ◽  
D. Davenne ◽  
S. Shoham ◽  
C. A. Dinarello ◽  
J. M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Temperature Changes ◽  
Arousal State ◽  
Intraventricular Infusion ◽  
Sleep Cycles

The effects of human interleukin 1 (IL 1) on the architecture of rabbit sleep-wake cycles and brain temperature (Tbr) changes coupled to states of vigilance were examined. Cerebral intraventricular infusion of IL 1 induced increased slow-wave sleep (SWS), increased electroencephalographic slow-wave (0.5-4 Hz) amplitudes, and fever. Heat-inactivated IL 1 failed to elicit these responses. IL 1 also significantly inhibited rapid-eye-movement (REM) sleep; however, inactivated IL 1 also reduced REM sleep; thus some of the IL 1-induced REM reduction may be related to the infusion process. The duration and number of sleep cycles (REM-to-REM interval) were unaffected by IL 1. Similarly, Tbr changes that normally occur during the transition from one arousal state to another remained unchanged after IL 1 infusion, even though rabbits were simultaneously febrile. We conclude that IL 1 selectively enhances SWS while leaving sleep cycles and Tbr changes coupled to states of vigilance undisturbed.

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.

Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep

1987 ◽  
Vol 253 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
S. Shoham ◽  
D. Davenne ◽  
A. B. Cady ◽  
C. A. Dinarello ◽  
J. M. Krueger
Keyword(s):  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Slow Wave ◽  
Tumor Necrosis ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Temperature Changes ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

The cytokines interleukin 1 (IL 1) and interferon (IFN) are immune response modifiers that are also pyrogenic and somnogenic. Tumor necrosis factor (TNF) (cachectin) is another pyrogenic monocyte product whose production can be elicited by somnogenic agents such as endotoxin. Human recombinant TNF (rTNF), therefore, was assayed for somnogenic activity. Intravenous (iv) or intracerebroventricular (ICV) injections of rTNF enhanced slow-wave sleep (SWS) and electroencephalographic slow-wave (0.5-4.0 Hz) activity. Recombinant TNF also suppressed rapid-eye-movement sleep (REM) and induced biphasic fevers whether given by intravenous or ICV injection. Responses to rTNF were compared with those elicited by human recombinant beta-IL 1 (rIL 1). Sleep responses elicited by rIL 1 were similar to those previously reported for native IL 1 and to those elicited by rTNF. However, unlike rTNF, rIL 1 induced monophasic fevers. Animal behavior and brain temperature changes that occur during the transition from one arousal state to another remained undisturbed after either rTNF or rIL 1 treatment. The fact that TNF and IL 1 as well as other immunoactive substances, e.g., IFN, muramyl peptides, and endotoxin, enhance SWS suggests that SWS is linked to the immune response. We conclude that TNF, in addition to IL 1 and IFN, is an endogenous somnogen.

Polyriboinosinic:polyribocytidylic acid enhances rabbit slow-wave sleep

1988 ◽  
Vol 255 (5) ◽  
pp. R748-R755 ◽  
Author(s):  
J. M. Krueger ◽  
J. A. Majde ◽  
C. M. Blatteis ◽  
J. Endsley ◽  
R. A. Ahokas ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Body Movement ◽  
Poly I:C ◽  
Viral Dsrna ◽  
Intracerebroventricular Injections ◽  
Effective Doses ◽  
Polyriboinosinic:Polyribocytidylic Acid ◽  
Dose Dependent

Drowsiness and fever are common symptoms of many viral diseases. It has been postulated that double-stranded RNA (dsRNA) produced during viral replication may cause these symptoms by direct toxic effects or by inducing interferon (IFN) or other cytokine production. Polyriboinosinic:polyribocytidylic acid (poly I:C), a pyrogenic and IFN-inducing synthetic dsRNA, and polyriboadenylic:polyribouridylic acid (poly A:U), a less effective pyrogen and IFN-inducing substance, were used as models of viral dsRNA to further characterize the physiological response to dsRNA. Poly I:C was injected either intravenously or intracerebroventricularly into rabbits, and electroencephalograph, body movement, and brain temperature were monitored over the next 6 h; blood samples were taken 24 h postinjection. Poly I:C increased slow-wave sleep duration, suppressed rapid-eye-movement sleep, and induced fever but failed to raise plasma Cu. Dose-dependent responses occurred after intravenous or intracerebroventricular injections; minimal effective doses were 0.3 micrograms/kg (iv) and 1.0 ng (icv). Poly A:U failed to alter the sleep or temperature parameters measured. Responses elicited by poly I:C were distinct from those elicited by bacterial products, e.g., endotoxin enhances plasma Cu levels, thus implying different mechanisms. We conclude that poly I:C enhances slow-wave sleep and body temperature without provoking the acute-phase rise in plasma Cu. These effects may be initiated through an IFN-mediated process.

Role of corticotropin-releasing hormone in stressor-induced alterations of sleep in rat

2002 ◽  
Vol 283 (2) ◽  
pp. R400-R407 ◽  
Author(s):  
Fang-Chia Chang ◽  
Mark R. Opp
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Physical Restraint ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
The Impact

Corticotropin-releasing hormone (CRH) mediates responses to a variety of stressors. We subjected rats to a 1-h period of an acute stressor, physical restraint, and determined the impact on subsequent sleep-wake behavior. Restraint at the beginning of the light period, but not the dark period, increased waking and reduced rapid eye movement sleep without dramatically altering slow-wave sleep (SWS). Electroencephalogram (EEG) slow-wave activity during SWS and brain temperature were increased by this manipulation. Central administration of the CRH receptor antagonist astressin blocked the increase in waking after physical restraint, but not during the period of restraint itself. Blockade of CRH receptors with astressin attenuated the restraint-induced elevation of brain temperature, but not the increase of EEG slow-wave activity during subsequent SWS. Although corticosterone increased after restraint in naive animals, it was not altered by this manipulation in rats well habituated to handling and injection procedures. These results suggest that under these conditions central CRH, but not the hypothalamic-pituitary-adrenal axis, is involved in the alterations in sleep-wake behavior and the modulation of brain temperature of rats exposed to physical restraint.

Cessation of thermoregulation during REM sleep in the pocket mouse

1983 ◽  
Vol 244 (1) ◽  
pp. R114-R118 ◽  
Author(s):  
J. M. Walker ◽  
L. E. Walker ◽  
D. V. Harris ◽  
R. J. Berger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Ground Squirrels ◽  
Rapid Eye Movement ◽  
Ambient Temperatures ◽  
Respiration Frequency ◽  
Pocket Mouse

Electrophysiological sleep patterns, respiration frequency, brain temperature (Tbr), and ear temperature (Tear) were recorded from five pocket mice (Perognathus longimembris) exposed to ambient temperatures (Ta) of 22.5, 27.5, 32.5, and 35.0 degrees C. Thermoregulation was curtailed during rapid-eye-movement (REM) sleep, since Tbr declined following REM onsets at Ta's below thermoneutrality and increased at Ta's above thermoneutrality. Tbr subsequently returned to pre-REM levels following the termination of each REM episode. Respiratory frequency was inversely related to Ta but not as strongly during REM sleep as during slow-wave sleep (SWS). These results confirm previous reports of loss of thermoregulatory ability during REM sleep. Mean duration and proportions of wakefulness, SWS, and REM sleep were unaffected by Ta, consistent with earlier findings on ground squirrels, but differing from reports of decreased REM sleep in nonhibernators. Hibernators may have lower peripheral thermosensitivities than nonhibernators, facilitating sleep at low ambient temperatures and during entrance into hibernation.

scholarly journals Modal-Polar Representation of Evoked Response Potentials in Multiple Arousal States

2021 ◽  
Vol 15 ◽  
Author(s):  
Rawan K. El-Zghir ◽  
Natasha C. Gabay ◽  
Peter A. Robinson
Keyword(s):  
Transfer Function ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Activity ◽  
Evoked Response ◽  
Temporal Part ◽  
Sleep State ◽  
Global Mode ◽  
Eyes Closed ◽  
Evoked Response Potentials

An expansion of the corticothalamic transfer function into eigenmodes and resonant poles is used to derive a simple formula for evoked response potentials (ERPs) in various states of arousal. The transfer function corresponds to the cortical response to an external stimulus, which encodes all the information and properties of the linear system. This approach links experimental observations of resonances and characteristic timescales in brain activity with physically based neural field theory (NFT). The present work greatly simplifies the formula of the analytical ERP, and separates its spatial part (eigenmodes) from the temporal part (poles). Within this framework, calculations involve contour integrations that yield an explicit expression for ERPs. The dominant global mode is considered explicitly in more detail to study how the ERP varies with time in this mode and to illustrate the method. For each arousal state in sleep and wake, the resonances of the system are determined and it is found that five poles are sufficient to study the main dynamics of the system in waking eyes-open and eyes-closed states. Similarly, it is shown that six poles suffice to reproduce ERPs in rapid-eye movement sleep, sleep state 1, and sleep state 2 states, whereas just four poles suffice to reproduce the dynamics in slow wave sleep. Thus, six poles are sufficient to preserve the main global ERP dynamics of the system for all states of arousal. These six poles correspond to the dominant resonances of the system at slow-wave, alpha, and beta frequencies. These results provide the basis for simplified analytic treatment of brain dynamics and link observations more closely to theory.

Somnogenic, pyrogenic, and hematologic effects of bacterial peptidoglycan

1990 ◽  
Vol 258 (1) ◽  
pp. R182-R186 ◽  
Author(s):  
L. Johannsen ◽  
L. A. Toth ◽  
R. S. Rosenthal ◽  
M. R. Opp ◽  
F. Obal ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Staphylococcus Aureus ◽  
Body Temperature ◽  
Slow Wave ◽  
Bacterial Cell ◽  
Cell Walls ◽  
Bacterial Infections ◽  
Slow Wave Sleep ◽  
Rapid Eye Movement Sleep ◽  
Bacterial Peptidoglycan

Bacterial infections and certain muramyl peptides elicit a variety of pathophysiological effects including increases in body temperature and slow-wave sleep. Bacterial cell wall peptidoglycan is composed of muramyl peptides. To investigate the ability of isolated bacterial cell walls to enhance slow-wave sleep, rabbits were injected intravenously with cell walls isolated from Staphylococcus aureus or with soluble peptidoglycan prepared from Neisseria gonorrhoeae. These injections increased slow-wave sleep, electroencephalographic delta-wave amplitudes, and body temperature, reduced rapid-eye-movement sleep, and induced neutrophilia and lymphopenia. The somnogenic and pyrogenic effects of S. aureus cell walls developed within 1 h and persisted throughout the recording period. Injections of N. gonorrhoeae peptidoglycan induced similar effects but of larger magnitude and shorter duration. We conclude that peptidoglycan is a bacterial component that mediates the increased sleep observed during infectious disease.

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