Central administration of neuropeptide Y induces wakefulness in rats

2006 ◽  
Vol 291 (2) ◽  
pp. R473-R480 ◽  
Author(s):  
E. Szentirmai ◽  
J. M. Krueger
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Eye Movement ◽  
Power Spectra ◽  
Physiological Saline ◽  
Rapid Eye Movement ◽  
Central Administration ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Routes Of Administration

Neuropeptide Y (NPY) is a well-characterized neuromodulator in the central nervous system, primarily implicated in the regulation of feeding. NPY, orexins, and ghrelin form a hypothalamic food intake regulatory circuit. Orexin and ghrelin are also implicated in sleep-wake regulation. In the present experiments, we studied the sleep-modulating effects of central administration of NPY in rats. Rats received intracerebroventricular injection of physiological saline or three different doses of NPY (0.4, 2, and 10 μg in a volume of 4 μl) at light onset. Another group of rats received bilateral microinjection of saline or 2 μg NPY in the lateral hypothalamus in a volume of 0.2 μl. Sleep-wake activity and motor activity were recorded for 23 h. Food intake after the control and treatment injections was also measured on separate days. Intracerebroventricular and lateral hypothalamic administration of NPY suppressed non-rapid-eye-movement sleep and rapid-eye-movement sleep in rats during the first hour after the injection and also induced changes in electroencephalogram delta power spectra. NPY stimulated food intake in the first hour after both routes of administration. Data are consistent with the hypothesis that NPY has a role in the integration of feeding, metabolism, and sleep regulation.

Electroencephalogram analysis of non-rapid eye movement sleep in rats

1988 ◽  
Vol 255 (1) ◽  
pp. R27-R37 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Power Spectra ◽  
Low Frequency ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Episode Duration ◽  
High Frequency Activity

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.

Epidermal growth factor enhances spontaneous sleep in rabbits

1998 ◽  
Vol 275 (2) ◽  
pp. R509-R514 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
Zutang Chen ◽  
Ying Wang ◽  
James M. Krueger
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Eye Movement ◽  
Brain Temperature ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Guide Cannula ◽  
Epidermal Growth

Several growth factors are implicated in sleep regulation. Epidermal growth factor (EGF) is found in the brain, and it influences the production of several sleep-promoting substances. We determined, therefore, whether administration of exogenous EGF affected spontaneous sleep in rabbits. Twenty-five rabbits were implanted with electroencephalographic electrodes, a brain thermistor, and an intracerebroventricular guide cannula. Three doses of EGF (0.5, 5, and 25 μg) were used. The animals were injected intracerebroventricularly with saline as control and one dose of EGF on 2 separate days. Five and twenty-five micrograms of EGF enhanced non-rapid eye movement sleep and increased brain temperature. The 25-μg dose of EGF also inhibited rapid eye movement sleep across the 23-h postinjection recording period. Results are consistent with the hypothesis that EGF, like other growth factors, could be involved in sleep regulation.

Varying photoperiod in the laboratory rat: profound effect on 24-h sleep pattern but no effect on sleep homeostasis

1995 ◽  
Vol 269 (3) ◽  
pp. R691-R701 ◽  
Author(s):  
P. Franken ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Pattern ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Marked Rise ◽  
Laboratory Rats

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.

Constant light suppresses sleep and circadian rhythms in pigeons without consequent sleep rebound in darkness

1994 ◽  
Vol 267 (4) ◽  
pp. R945-R952 ◽  
Author(s):  
R. J. Berger ◽  
N. H. Phillips
Keyword(s):  
Circadian Rhythms ◽  
Eye Movement ◽  
Power Spectra ◽  
Behavioral Changes ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Patterns ◽  
Free Running ◽  
Dim Light ◽  
Dd Transitions

Sleep patterns and circadian rhythms of body temperature, activity, body weight, and electroencephalographic (EEG) power spectra of pigeons were compared among three photic conditions: a 12:12-h light-dark cycle (LD), followed successively by constant bright (LL) and dim light (DD) periods. LL suppressed non-rapid-eye-movement and rapid eye movement sleep and circadian rhythms of the measured variables without producing increased drowsiness or other physiological or behavioral changes. Sleep patterns after LL-DD transitions also showed no evidence of prior sleep deprivation during LL. Sleep latency after LL-DD transitions was 93 min longer than after L-D transitions in LD. Total sleep and EEG slow wave activity during the first 24 h in DD did not differ from D in LD. Free-running circadian rhythms subsequently reappeared in DD after LL.

Neuropeptide-Y Y2-receptor agonist, PYY3–36 promotes non-rapid eye movement sleep in rat

2006 ◽  
Vol 54 (3) ◽  
pp. 165-170 ◽  
Author(s):  
Moses A. Akanmu ◽  
Otas E. Ukponmwan ◽  
Yoshifumi Katayama ◽  
Kazuki Honda
Keyword(s):  
Neuropeptide Y ◽  
Eye Movement ◽  
Receptor Agonist ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Y2 Receptor

Growth hormone-releasing hormone: cerebral cortical sleep-related EEG actions and expression

2007 ◽  
Vol 293 (2) ◽  
pp. R922-R930 ◽  
Author(s):  
Éva Szentirmai ◽  
Tadanobu Yasuda ◽  
Ping Taishi ◽  
Mingxiang Wang ◽  
Lynn Churchill ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Eye Movement ◽  
Wave Power ◽  
Growth Hormone Releasing Hormone ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Delta Wave ◽  
Releasing Hormone ◽  
Delta Power

Growth hormone-releasing hormone (GHRH), its receptor (GHRHR), and other members of the somatotropic axis are involved in non-rapid eye movement sleep (NREMS) regulation. Previously, studies established the involvement of hypothalamic GHRHergic mechanisms in NREMS regulation, but cerebral cortical GHRH mechanisms in sleep regulation remained uninvestigated. Here, we show that unilateral application of low doses of GHRH to the surface of the rat somatosensory cortex ipsilaterally decreased EEG delta wave power, while higher doses enhanced delta power. These actions of GHRH on EEG delta wave power occurred during NREMS but not during rapid eye movement sleep. Further, the cortical forms of GHRH and GHRHR were identical to those found in the hypothalamus and pituitary, respectively. Cortical GHRHR mRNA and protein levels did not vary across the day-night cycle, whereas cortical GHRH mRNA increased with sleep deprivation. These results suggest that cortical GHRH and GHRHR have a role in the regulation of localized EEG delta power that is state dependent, as well as in their more classic hypothalamic role in NREMS regulation.

Tumor necrosis factor-beta induces sleep, fever, and anorexia

1992 ◽  
Vol 263 (3) ◽  
pp. R703-R707 ◽  
Author(s):  
L. Kapas ◽  
J. M. Krueger
Keyword(s):  
Food Intake ◽  
Tumor Necrosis Factor ◽  
Eye Movement ◽  
Tumor Necrosis ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Necrosis Factor

The enhanced sleep, fever, and anorexia experienced during general infections are attributed to the increased production of cytokines. Cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) have characteristic somnogenic, pyrogenic, and anorectic effects. TNF-beta is closely related to TNF-alpha, and they share common receptors. The effects of TNF-beta on sleep-wake activity, brain temperature (Tbr), and food intake were, however, heretofore unknown. We injected 0.5-200 ng TNF-beta into rabbits intracerebroventricularly (icv) in the light period, and the electroencephalogram, movement, and Tbr were recorded for 6 h from rabbits. The highest dose, 200 ng TNF-beta, induced increases in non-rapid-eye-movement sleep and decreases in rapid-eye-movement sleep accompanied with biphasic febrile responses. Icv injection of 100 ng TNF-beta at dark onset suppressed 12-h and 24-h food intake in rats. These data suggest to us that TNF-beta may belong to the group of endogenous pyrogens/sleep factors.

Nuclear factor-κB inhibitor peptide inhibits spontaneous and interleukin-1β-induced sleep

2000 ◽  
Vol 279 (2) ◽  
pp. R404-R413 ◽  
Author(s):  
Takeshi Kubota ◽  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Nuclear Factor Κb ◽  
Current Data ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Cytokine Network ◽  
Inhibitor Peptide

Nuclear factor-κB (NF-κB) is a transcription factor that when activated promotes production of several sleep-promoting substances such as interleukin-1β (IL-1β), tumor necrosis factor-α, and nerve growth factor. Therefore, we hypothesized that inhibition of NF-κB activation would attenuate sleep. A NF-κB cell-permeable inhibitor peptide (IP) was injected intracerebroventricularly (5 and 50 μg for rats, 100 μg for rabbits). On a separate day, time-matched control injections of a cell-permeable inactive control peptide were done in the same animals. The 50-μg dose of IP in rats and the 100-μg dose in rabbits significantly inhibited non-rapid eye movement sleep and rapid eye movement sleep if administered during the light period. Moreover, pretreatment of rabbits with 100 μg of the IP 12 h before intracerebroventricular injection of IL-1β (10 ng) significantly attenuated IL-1β-induced sleep and febrile responses. The current data support the hypothesis that a brain cytokine network is involved in sleep regulation and that NF-κB is a crucial factor in physiological sleep regulation.

Interleukin-4 inhibits spontaneous sleep in rabbits

1998 ◽  
Vol 275 (4) ◽  
pp. R1185-R1191 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
Ying Wang ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Interleukin 4 ◽  
Light Cycle ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Cytokine Network ◽  
Factor Α ◽  
Physiological Sleep ◽  
Necrosis Factor

Proinflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α, are involved in sleep regulation. IL-4 is an antiinflammatory cytokine that inhibits proinflammatory cytokine production. The hypothesis that IL-4 should attenuate sleep was studied by determining the effects of IL-4 on rabbit spontaneous sleep. Thirty-six rabbits were used. Four doses of IL-4 (0.25, 2.5, 25, and 250 ng) were injected intracerebroventricularly during the rest (light) period. One dose of IL-4 (25 ng) was injected during the active (dark) cycle. Appropriate time-matched control injections of saline were done in the same rabbits on different days. The three highest doses of IL-4 significantly inhibited spontaneous non-rapid eye movement sleep if IL-4 was given during the light cycle. The highest dose of IL-4 (250 ng) also significantly decreased rapid eye movement sleep. On the other hand, IL-4 administered at dark onset had no effect on sleep. The sleep inhibitory properties of IL-4 provide additional evidence for the hypothesis that a brain cytokine network is involved in the regulation of physiological sleep.

Sign in / Sign up

Export Citation Format

Share Document