Increased interictal spike activity associated with transient slow wave trains during non-rapid eye movement sleep

2014 ◽  
Vol 13 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Péter Przemyslaw Ujma ◽  
Péter Simor ◽  
Raffaele Ferri ◽  
Dániel Fabó ◽  
Anna Kelemen ◽  
...  
2003 ◽  
Vol 285 (1) ◽  
pp. R99-R109 ◽  
Author(s):  
Hitoshi Yoshida ◽  
Takeshi Kubota ◽  
James M. Krueger

Sleep is regulated in part by the brain cytokine network, including tumor necrosis factor-α (TNF-α). TNF-α activates the transcription factor nuclear factor-κB, which in turn promotes transcription of many genes, including cyclooxygenase-2 (COX-2). COX-2 is in the brain and is an enzyme responsible for production of prostaglandin D2. The hypothesis that central COX-2 plays a role in the regulation of spontaneous and TNF-α-induced sleep was investigated. Three doses (0.5, 5, and 50 μg) of NS-398, a highly selective COX-2 inhibitor, were injected intracerebroventricularly. The highest dose decreased non-rapid eye movement sleep. The intermediate and highest doses decreased electroencephalographic slow-wave activity; the greatest reduction occurred after 50 μg of NS-398 during the first 3-h postinjection period. Rapid eye movement sleep and brain temperature were not altered by any dose of NS-398. Pretreatment of rabbits with 5 or 50 μg of NS-398 blocked the TNF-α-induced increases in non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature. These data suggest that COX-2 is involved in the regulation of spontaneous and TNF-α-induced sleep.


1988 ◽  
Vol 255 (1) ◽  
pp. R27-R37 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely

Sleep states and power spectra of the electroencephalogram were determined for consecutive 4-s epochs during 24 h in rats that had been implanted with electrodes under deep pentobarbital anesthesia. The power spectra in non-rapid eye movement sleep (NREMS) showed marked trends: low-frequency activity (0.75-7.0 Hz) declined progressively throughout the 12-h light period (L) and remained low during most of the 12-h dark period (D); high-frequency activity (10.25-25.0 Hz) rose toward the end of L and reached a maximum at the beginning of D. Within a single NREMS episode (duration 0.5-5.0 min), slow-wave activity (0.75-4.0 Hz) increased progressively to a plateau level. The rise was approximated by a saturating exponential function: although the asymptote level of the function showed a prominent 24-h rhythm, the time constant remained relatively stable (approximately 40 s). After short interruptions of NREMS episodes, slow-wave activity rose more steeply than after long interruptions. The marked 24-h variation of maximum slow-wave activity within NREMS episodes may reflect the level of a homeostatic sleep process.


Author(s):  
Wei Jing ◽  
Yanran Wang ◽  
Guangzhan Fang ◽  
Mingming Chen ◽  
Miaomiao Xue ◽  
...  

1981 ◽  
Vol 241 (4) ◽  
pp. E269-E274
Author(s):  
J. E. Garcia-Arraras

Slow-wave sleep (SWS) and rapid-eye-movement sleep (REM) were recorded in cats for 32 h a) under control conditions, b) following intraventricular infusions of artificial cerebrospinal fluid (CSF), and c) following infusions of sleep-promoting factor S prepared from human urine (SPU). During the first 12 h after receiving artificial CSF, the cats slept 4.9 +/- 0.2 h in slow-wave sleep (SWS) and 1.4 +/- 0.1 h in REM. Similar values were obtained from the same cats under control conditions. After infusions of SPU, the duration of SWS in the same cats increased to an average of 6.9 +/- 0.5 h with no significant change in REM averaged over 12 h; a transient decrease of REM in the first 4 h was fully compensated in subsequent hours. The increased SWS induced by the sleep-promoting factor from human urine subsided after 12 h, and there was no compensatory increase in wakefulness during the subsequent 20 h. The normal sleep cycle was not affected. In cats, therefore, the primary effect of SPU is to increase normal SWS, with little effect on REM.


2003 ◽  
Vol 94 (3) ◽  
pp. 883-890 ◽  
Author(s):  
Michael F. Fitzpatrick ◽  
Helen S. Driver ◽  
Neela Chatha ◽  
Nha Voduc ◽  
Alison M. Girard

The oral and nasal contributions to inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 ± 5 yr, with normal nasal resistance (mean 2.0 ± 0.3 cmH2O · l−1 · s−1) by use of a divided oral and nasal mask. Minute ventilation awake (5.9 ± 0.3 l/min) was higher than that during sleep (5.2 ± 0.3 l/min; P < 0.0001), but there was no significant difference in minute ventilation between different sleep stages ( P = 0.44): stage 2 5.3 ± 0.3, slow-wave 5.2 ± 0.2, and rapid-eye-movement sleep 5.2 ± 0.2 l/min. The oral fraction of inhaled ventilation during wakefulness (7.6 ± 4%) was not significantly different from that during sleep (4.3 ± 2%; mean difference 3.3%, 95% confidence interval −2.1–8.8%, P = 0.19), and no significant difference ( P = 0.14) in oral fraction was observed between different sleep stages: stage two 5.1 ± 2.8, slow-wave 4.2 ± 1.8, rapid-eye-movement 3.1 ± 1.7%. Thus the inhaled oral fraction in normal subjects is small and does not change significantly with sleep stage.


2019 ◽  
Vol 79 (3) ◽  
pp. 252-261
Author(s):  
Acharaporn Issuriya ◽  
Ekkasit Kumarnsit ◽  
Chayaporn Reakkamnuan ◽  
Nifareeda Samerphob ◽  
Pornchai Sathirapanya ◽  
...  

1995 ◽  
Vol 269 (3) ◽  
pp. R691-R701 ◽  
Author(s):  
P. Franken ◽  
I. Tobler ◽  
A. A. Borbely

To assess the influence of the photoperiod on sleep regulation, laboratory rats were adapted to a long photoperiod (LPP; 16:8-h light-dark cycle, LD 16:8) or a short photoperiod (SPP; LD 8:16). The electroencephalogram (EEG) and cortical temperature (TCRT) were continuously recorded for a baseline day, a 24-h sleep deprivation (SD) period, and a recovery day. Data obtained previously for LD 12:12 served for comparison. Whereas the photoperiod exerted a prominent effect on the 24-h sleep pattern, the 24-h baseline level of sleep and the response to SD were little affected. Recovery from SD was characterized by a marked rise in rapid eye movement sleep, a moderate rise in non-rapid eye movement sleep, and an initial enhancement of EEG slow-wave activity followed by a decrease below baseline. The amplitude and phase of the "unmasked" 24-h component of TCRT did not differ between LPP and SPP. Computer simulations demonstrated that the changes of TCRT and EEG slow-wave activity can be largely accounted for by the sequence of the vigilance states. We conclude that the photoperiod does not affect the basic processes underlying sleep regulation.


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