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D Stenberg

Publications and source records attributed to D Stenberg.

At least 19 recordsLinked to original sources
PubMed2000

Intracerebroventricular and locus coeruleus microinjections of somatostatin antagonist decrease REM sleep in rats.

In order to study the role of endogenous somatostatin in the physiologic modulation of REM sleep (REMS), we measured the effect of intracerebroventricular (ICV) injection of somatostatin antagonist (SA) cyclo-(7-aminoheptanoyl-phe-d-trp-lys-thr(bzl)) on sleep in rats. The effect of ICV SA was also tested after 24-h REMS deprivation with the platform method. To study the role of locus coeruleus (LC) as a site of the sleep inducing action for somatostatin and galanin we microinjected SA, somatostatin, and galanin locally into LC. In all experiments, vigilance state was analyzed visually from 6 h post-injection EEG/EMG recording. Injection of 0.5 and 2 nmol of SA ICV reduced spontaneous REMS and 2 nmol dose reduced also rebound REMS after REMS deprivation when compared with controls (artificial cerebrospinal fluid vehicle). Microinjection of 0.25 nmol of SA into LC reduced REMS, whereas microinjection of somatostatin, galanin, and a combined injection of them were not effective to induce REMS. The results suggest that endogenous somatostatin may contribute to facilitation of REMS. Somatostatin receptors in the LC may be one possible mediator of this effect.

Animals↗
PubMed1999

Adenosine and behavioral state control: adenosine increases c-Fos protein and AP1 binding in basal forebrain of rats.

In several brain areas, extracellular adenosine (AD) levels are higher during waking than sleep and during prolonged wakefulness AD levels in the basal forebrain increase progressively. Similarly, c-Fos levels in several brain areas are higher during waking than sleep and remain elevated during prolonged wakefulness. In the present study, we investigated the effect of extracellular AD levels on c-Fos protein and activator protein-1 (AP1) binding in the basal forebrain of rats. Increased levels of extracellular AD were induced either by keeping the animals awake, or by local perfusion of AD into the basal forebrain. During prolonged wakefulness extracellular AD concentration was monitored using in vivo microdialysis. The effect of AD perfusion on the behavioral states was recorded using polysomnography. At the end of the perfusion period the basal forebrain tissue was analyzed for the levels of c-Fos protein and AP1 binding. In vivo microdialysis measurements showed an increase in AD levels with prolonged wakefulness. Unilateral perfusion of AD (300 microM) increased non-REM sleep and delta power (0.5 to 4 Hz) when compared to rats perfused with artificial CSF. The levels of c-Fos protein and the AP1 DNA binding were high in the basal forebrain of both sleep-deprived animals and in animals perfused with AD. The results suggest that AD might mediate, at least in part, the long term effects of sleep deprivation by inducing c-Fos protein and subsequent AP1 binding.

Adenosine↗
PubMed1997

Sleep deprivation increases brain serotonin turnover in the rat.

IN order to study possible time-dependent changes in serotonin metabolism in rat brain, male Wistar rats were subjected to 3, 6 or 12 h total sleep deprivation (SD) by gentle handling. In addition two groups of rats subjected first to 6 h SD were allowed 2 or 4 h rebound sleep. Tissue concentrations of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured from several brain areas using HPLC/ECD. SD significantly increased the 5-HIAA/5-HT ratio in frontal cortex, hippocampus, hypothalamus and brain stem, indicating increased 5-HT turnover in those areas. After 2 and 4 h rebound sleep, the 5-HIAA/5-HT ratio was similar to that in controls. We conclude that a short SD increases 5-HT turnover in the rat brain for the duration of SD only.

Animals↗
PubMed1997

Sleep deprivation increases somatostatin and growth hormone-releasing hormone messenger RNA in the rat hypothalamus.

We studied the effect of sleep deprivation (SD) on the amount of somatostatin (SRIF) and growth hormone-releasing hormone (GHRH) mRNA in rat hypothalamic nuclei. According to earlier studies SRIF possibly facilitates REM sleep and GHRH slow-wave sleep. Adult male rats were sleep deprived by the gentle handling method either for 6 h during the first half of the light phase or for 12 h during the dark phase. Undisturbed rats sacrificed at the same time as the SD rats served as controls. After oligonucleotide in situ hybridization the amount of SRIF and GHRH mRNA was measured in brain sections by image analysis and cell count. SD increased the amount of SRIF mRNA in the arcuate nucleus (ARC). In the periventricular nucleus (PE) there was no effect. The amount of GHRH mRNA increased in the paraventricular nucleus (PA) in the 6 h SD group but no effect was detected in ARC. In the periventromedial hypothalamic area (pVMH) the amount of GHRH mRNA was higher in the control rats sacrificed in the morning (09.00 hours) than in the afternoon (15.00 hours), and SD had no effect. We conclude that SRIF cells in ARC and GHRH cells in PA are modulated by sleep loss, which is in accordance with the possible sleep regulatory function of these neuropeptides.

Animals↗
PubMed1996

The effect of REM sleep deprivation on somatostatin and growth hormone-releasing hormone gene expression in the rat hypothalamus.

Growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) have been implicated as sleep factors. We studied how the hypothalamic SRIF/GHRH system is affected by possible feedback regulation resulting from REM sleep deprivation at the level of gene expression and how this is reflected in serum growth hormone (GH) content. Male rats were deprived of REM sleep on small platforms for 24 or 72 h, and one group was allowed a rebound sleep of 24 h after 72 h deprivation. Animals maintained on large platforms and animals taken directly from their home cages served as controls. In situ hybridization was made from 20 microm cryosections through the periventricular, paraventricular and arcuate hypothalamic nuclei using oligonucleotide probes for GHRH and SRIF. The number of cells expressing SRIF or GHRH was counted. Serum GH was measured by means of radioimmunoassay in similarly treated rats. Fewer cells expressed GHRH in the paraventricular nucleus of animals subjected to 24 and 72 h of REM sleep deprivation than in home control animals. A similar trend was observed in the arcuate nucleus. The number of cells expressing SRIF was elevated in the arcuate nucleus after 24 h of REM sleep deprivation but not after 72 h. In the periventricular nucleus the number of cells expressing SRIF was higher after 72 h of deprivation when compared to expression in animals maintained on large platforms. Serum GH levels were decreased in animals maintained on either small or large platforms. It is concluded that the expression of the SRIF and GHRH genes is modulated by REM sleep deprivation.

Animals↗
PubMed1995

Sleep deprivation increases brain serotonin turnover in the Djungarian hamster.

Djungarian hamsters well adapted to a short photoperiod were subjected to 4 h of total sleep deprivation (SD) by gentle handling. Tissue concentrations of monoamines and of their metabolites were measured from several brain areas using HPLC with electrochemical detection. The 5-hydroxyindoleacetic acid/5-hydroxytryptamine (5-HIAA/5-HT) ratio was significantly increased after SD in the hippocampus, hypothalamus and brain stem, indicating increased serotonin (5-HT) turnover in those areas, while no changes were found in the frontal cortex and olfactory bulb. Dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations were elevated in the hypothalamus, while the noradrenaline concentrations did not change in any of the measured areas. We conclude that a short SD, which has been shown to elevate EEG slow-wave activity during recovery sleep, specifically increases 5-HT turnover in the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

REM sleep deprivation induces galanin gene expression in the rat brain.

Rats were deprived of REM sleep for 24 h by keeping them on small platforms that were placed in a water bath (the platform method). Galanin coding mRNA was visualized using in situ hybridization, and cells expressing galanin mRNA were counted. In REM sleep-deprived animals the cell count was higher in the preoptic area and periventricular nucleus. Lesions of this area have been reported to induce wakefulness in cats and rats. Galanin administered into the lateral ventricle had no effect on sleep. We conclude that REM sleep deprivation can induce galanin gene expression in some brain areas, but galanin alone does not modify spontaneous sleep.

Animals↗
PubMed1995

Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep.

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.

Animals↗
PubMed1994

The effect of REM sleep deprivation on histamine concentrations in different brain areas.

Rats were deprived of REM sleep (REMS) for 72 h with the platform method and decapitated in the morning immediately after the deprivation or in the afternoon after having been allowed 5 hours of rebound sleep. The histamine concentrations of the anterior and posterior hypothalamus, the cortex, the hippocampus and the pineal gland were measured, as well as the tele-methylhistamine concentrations of the anterior and posterior hypothalamus. Histamine concentrations were no different after REMS deprivation compared to large platform or dry cage controls, but in the anterior hypothalamus histamine levels increased during rebound sleep only in the REMS deprived rats. tele-Methylhistamine/histamine ratios were higher after 72 h of both REMS deprivation and the large platform treatment compared to dry cage controls, indicating increased histamine utilization during the platform treatment procedure.

Analysis of Variance↗
PubMed1994

Twenty-four-hour rhythms in relation to the natural photoperiod: a field study in humans.

The daily rhythms of salivary melatonin, salivary cortisol, and axillary body temperature were measured in nine healthy volunteers in midsummer, around the autumn equinox, and in midwinter, at a latitude of 60 degrees N. The aim was to find out whether these rhythms were dependent on variations of the natural daylength. The samples were collected every 2 hr during 24-hr periods in everyday conditions. The individual rhythms were characterized with the acrophase estimates of the best-fitting cosine curve models and with the half-rise and half-decline times calculated from the raw data. The melatonin and cortisol rhythms were delayed significantly (about 1 hr) in midwinter as compared with summer and autumn. The most advanced rhythms were found in autumn. The shifts of the melatonin and cortisol rhythms could be explained as a result of the changes of natural illumination. The overt temperature rhythms did not differ significantly among the sampling months. The lack of seasonal patterns in temperature rhythms probably primarily reflected the socially determined rest-activity cycles of the subjects.

Adult↗
PubMed1993

Alpha 2-adrenoceptors and vigilance in cats: antagonism of medetomidine sedation by atipamezole.

In order to evaluate the effect of a specific alpha 2-adrenoceptor antagonist, atipamezole, on vigilance, adult cats with implanted electrodes for polygraphy were tested in a double-blind Latin square design. The standard clinical dose (0.1 mg/kg i.m.) of the specific alpha 2-adrenoceptor agonist, medetomidine, promptly induced stuporous sedation. Atipamezole, given 30 min later at 0.2, 0.4 or 0.8 mg/kg i.m., reversed the sedation within 3 min, resulting in complete awareness of the animal. After the small dose of atipamezole, arousal with some motor excitation continued for 6 h, whereas after the larger doses, the physiological sleep-wake cycle returned earlier. Used alone, the preferred dose, 0.4 mg/kg atipamezole i.m., allowed physiological sleep within 33 +/- 9 min, compared to 22 +/- 3 min after saline. Atipamezole thus proved to be a most effective antagonist to sedation with alpha 2-adrenoceptor agonist drugs, without disturbing excitatory effects. Specific alpha 2-adrenoceptor modulating drugs have evident clinical application, as antidotes to overdosage of alpha 2-adrenoceptor agonists, or to terminate their effect after surgical procedures.

Adrenergic alpha-Agonists↗
PubMed1993

One-hour exposure to moderate illuminance (500 lux) shifts the human melatonin rhythm.

Salivary melatonin levels were measured in 12 healthy volunteers in order to determine whether a moderate light intensity, which suppresses the nocturnal rise of melatonin, was able to shift the melatonin rhythm. The samples were collected at 1-hr intervals under lighting of < 100 lux (experiment 1) or < 10 lux (experiment 2). The control melatonin profiles were determined during the first night. In the second night the subjects were exposed to light of 500 lux for 60 min during the rising phase of melatonin synthesis. The third series of samples was collected during the third night. The mean decrease of melatonin levels by the exposure to light was 56% of the prelight concentrations. The melatonin onset times were delayed significantly (about 30 min) the night after the exposure to light. The melatonin offset times tended to be delayed in experiment 2. The shifts of the melatonin offset correlated positively with the amount of the melatonin suppression. The results suggest that a relatively small and short lasting light-induced interruption of melatonin synthesis may affect the melatonin rhythm in humans.

Adult↗
PubMed1992

Pineal melatonin and locomotor activity of rats under gradual illuminance transitions.

The locomotor activity and pineal melatonin patterns of adult male rats were compared under two different lighting regimes. The animals were kept 8 days under 12/12 h light/dark cycles with abrupt or slowly decreasing and increasing transitions (twilight periods about 2 h). The onsets of high activity and melatonin rise were phase-locked in the two conditions and related to about half-maximal illuminance level of the gradual dusk. The high activity of the control rats stopped 30-60 min before the abrupt light onset and the rats under the gradual lighting transitions ceased the locomotor activity at about 1 hour before the half-maximal illuminance. The melatonin peak levels were found 4 h before the abrupt lights-on time. Under the slow illuminance transitions the average melatonin peak was related to the illuminance level between maximum and minimum in the morning. Thus, both the melatonin rhythm and the rest-activity rhythm under the gradual dawn and dusk were adjusted according to about half-maximal illuminances in the present conditions.

Animals↗
PubMed1992

The effect of testosterone on serum gonadotropins of castrated rats kept under different lighting conditions.

Testosterone feedback sensitivity was measured as the ability of testosterone propionate to decrease serum LH and FSH of long-term castrated (4 wk) rats under four different lighting conditions: periodic light (12L:12D), constant light (LL), constant darkness (DD), and dim night illumination (1 lx) with a 12L:12D photoperiod. Rats were exposed to the different lighting conditions for 1 wk, during which they received daily testosterone propionate (125 micrograms or 250 micrograms s.c.). At the end of the experiment the rats were decapitated at 1100 h, and serum gonadotropin levels were measured by RIA. Serum LH of the rats kept under LL was reduced to the level of the intact rats with the smaller testosterone dose (125 micrograms/day). Under all other lighting conditions only the large dose (250 micrograms/day) was able to restore the serum LH concentration to the level of the intact rats. Serum FSH was restored only partially, and the effect was the same with both doses and similar under all lighting conditions. We conclude that the increase in testosterone negative feedback sensitivity was not caused by the lack of periodicity of illumination alone, but that sufficient intensity of lighting throughout the 24 h was needed as well.

Animals↗
PubMed1992

Increase in testosterone sensitivity induced by constant light in relation to melatonin injections in rats.

In this experiment we investigated whether the lack of the nocturnal melatonin peak under constant light would cause an increase in testosterone sensitivity. Castrated rats were kept under periodic or constant light for one week. They received a daily injection of vehicle, testosterone propionate (125 micrograms), melatonin (50 micrograms) or testosterone plus melatonin (125 micrograms + 50 micrograms). Serum and pituitary gonadotrophins and pineal melatonin were measured at the end of the experiment. Under constant light, testosterone injections reduced the serum luteinizing hormone concentration in castrated rats to that in intact rats, but, under periodic light, the decrease was smaller. Melatonin did not reverse the stronger effect of testosterone under constant light. The serum melatonin peak produced by the exogenous melatonin injection had a higher amplitude, shorter duration and earlier appearance than the physiological melatonin peak. Exogenous melatonin did not modify the physiological melatonin secretion, measured either as serum melatonin concentration or pineal melatonin content on the consecutive day. We conclude that the increase in testosterone negative feedback sensitivity of castrated rats under constant light was not due to the absence of the nocturnal melatonin pulse.

Animals↗
PubMed1990

Daily melatonin injections have only minor effects on gonadotropins of intact or castrated male rats kept under constant or periodic light.

Intact and castrated adult male Wistar rats were kept under constant or periodic (lights on 0600 and off 1800 h) light for 1 wk. During the study they received melatonin or saline injections daily either at 0900 or 1600 h. After each experiment, serum samples and the adenohypophyses were collected between 1000 and 1100 h and the gonadotropin concentrations were measured radioimmunologically. We had previously found changes in light sensitivity of the hypothalamo-pituitary axis of castrated rats and hypothesized that this axis could also involve changes in sensitivity to exogenous melatonin. However, the results of the present study do not support the hypothesis.

Analysis of Variance↗