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O Van Reeth

Publications and source records attributed to O Van Reeth.

At least 19 recordsLinked to original sources
PubMed2003

Prenatal stress in rats predicts immobility behavior in the forced swim test. Effects of a chronic treatment with tianeptine.

Prenatally-stressed (PS) rats are characterized by a general impairment of the hypothalamo-pituitary-adrenal (HPA) axis and sleep disturbances indicating that this model has face validity with some clinical features observed in a subpopulation of depressed patients. The prolonged corticosterone secretion shown by PS rats in response to stress was positively correlated with an increased immobility behavior in the forced swim test. To investigate the predictive validity of this model, a separate group of animals was chronically treated with the antidepressant tianeptine (10 mg/kg i.p. for 21 days). Such chronic treatment reduced in PS rats immobility time in the forced swim test. These findings suggest that the PS rat is an interesting animal model for the evaluation of antidepressant treatment.

Analysis of Variance↗
PubMed2002

Circadian clock functioning is linked to acute stress reactivity in rats.

At least two major physiological systems are involved in the adaptation of the organism to environmental challenges: the circadian system and the stress reaction. This study addressed the possibility that interindividual differences in stress sensitivity and in the functioning of the circadian system are related. At 2 months of age, corticosterone secretion in response to a 20-min restraint stress was assessed in 9 Sprague-Dawley rats for which running wheel activity was recorded as a rhythmic behavioral marker of the circadian clock. Two weeks later, the adaptive response of the circadian system to an abrupt shift in the light:dark (LD) cycle was assessed in those rats using a jet-lag paradigm. Finally, after resynchronization to the new LD cycle, rats were transferred to constant darkness to assess the free-running period of their circadian rhythm of running-wheel activity. Results indicate that stress-induced corticosterone secretion was (1) positively correlated with the number of days to resynchronize the circadian activity rhythm to the new LD cycle, and with the value of its free-running period, and (2) negatively correlated with the intensity of daily locomotor activity. Those data, emphasizing the interactions between the stress response of an organism and the functioning of its circadian system, could explain interindividual differences in humans' susceptibility to shift work or other circadian-related disorders.

Acute Disease↗
PubMed2002

[Fatigue and sleep: the point of view of the chronobiologist].

Chrono-fatigue is often present in patients engaged in shift or night work, as well as in passengers travelling across many time zones (jet lag syndrome). Some disturbances of the circadian system are responsible for clinical syndromes characterized by chrono-fatigue, one of them being the sleep delayed phase insomnia. Circadian sleep disorders, either functional or structural, are characterized not only by disturbances in sleep architecture and/or sleep quality, but also by the inability to fall asleep and stay awake at desired times. Similarly, sleep and fatigue present in those circadian disorders typically exhibit a daily cyclic pattern. Night workers and shift workers do have chronic sleep deprivation and desynchronisation of their circadian system with the entraining environment. Those phenomena are responsible for severe vigilance problems, a decrease in work productivity and deleterious health side effects. Fatigue and sleep problems in circadian disorders can now benefit from treatments based on the programed use of synchronizers of the circadian clock, like chronotherapy, bright light and melatonin, combined with adequate sleep hygiene recommendations.

Chronobiology Phenomena↗
PubMed2001

Sleep deprivation decreases phase-shift responses of circadian rhythms to light in the mouse: role of serotonergic and metabolic signals.

The circadian pacemaker in the suprachiasmatic nuclei is primarily synchronized to the daily light-dark cycle. The phase-shifting and synchronizing effects of light can be modulated by non-photic factors, such as behavioral, metabolic or serotonergic cues. The present experiments examine the effects of sleep deprivation on the response of the circadian pacemaker to light and test the possible involvement of serotonergic and/or metabolic cues in mediating the effects of sleep deprivation. Photic phase-shifting of the locomotor activity rhythm was analyzed in mice transferred from a light-dark cycle to constant darkness, and sleep-deprived for 8 h from Zeitgeber Time 6 to Zeitgeber Time 14. Phase-delays in response to a 10-min light pulse at Zeitgeber Time 14 were reduced by 30% in sleep-deprived mice compared to control mice, while sleep deprivation without light exposure induced no significant phase-shifts. Stimulation of serotonin neurotransmission by fluoxetine (10 mg/kg), a serotonin reuptake inhibitor that decreases light-induced phase-delays in non-deprived mice, did not further reduce light-induced phase-delays in sleep-deprived mice. Impairment of serotonin neurotransmission with p-chloroamphetamine (three injections of 10 mg/kg), which did not increase light-induced phase-delays in non-deprived mice significantly, partially normalized light-induced phase-delays in sleep-deprived mice. Injections of glucose increased light-induced phase-delays in control and sleep-deprived mice. Chemical damage of the ventromedial hypothalamus by gold-thioglucose (600 mg/kg) prevented the reduction of light-induced phase-delays in sleep-deprived mice, without altering phase-delays in control mice. Taken together, the present results indicate that sleep deprivation can reduce the light-induced phase-shifts of the mouse suprachiasmatic pacemaker, due to serotonergic and metabolic changes associated with the loss of sleep.

Animals↗
PubMed2001

Melatonin or a melatonin agonist corrects age-related changes in circadian response to environmental stimulus.

The effects of a melatonin agonist, S-20098, included in the diet were tested on a specific effect of aging in hamsters: the marked decline in the phase shifting effects of a 6-h pulse of darkness on a background of constant light. In contrast to young hamsters, old hamsters fed with the control diet showed little or no phase shifts in response to a dark pulse presented in the middle of their inactive or active period. Old hamsters fed with S-20098 showed phase shifts that were ~70% of the ones in young animals and significantly greater than those in old controls. The phase advancing response to a dark pulse presented during the inactive period was dose dependent and reversed after S-20098 discontinuation. Melatonin included in the diet showed comparable restorative effects on the phase shifting response to a dark pulse in old hamsters. Replacement therapy with melatonin or melatonin-related compounds could prove useful in treating, preventing, or delaying disturbances of circadian rhythmicity and/or sleep in older people.

Acetamides↗
PubMed2000

A melatonin agonist facilitates circadian resynchronization in old hamsters after abrupt shifts in the light-dark cycle.

Age-related changes in the mammalian circadian system may be associated with a decline in circulating melatonin levels. Using 'jet lag' paradigms involving abrupt shifts in the light-dark cycle, we showed that a melatonin agonist, S-20098, accelerated by approximately 25% resynchronization of the circadian activity rhythm in old hamsters to the new light-dark cycle. It suggests the usefulness of melatonin-related compounds to treat circadian disorders associated with aging.

Acetamides↗
PubMed2000

Sleep in the Wistar-Kyoto rat, a putative genetic animal model for depression.

The Wistar-Kyoto (WKY) rat exhibits several behavioral and hormonal abnormalities often associated with depression. One of the hallmarks of depression consists of alterations in the sleep-wake cycle, particularly in rapid eye movement (REM) sleep. If the WKY rat is indeed an animal model for depression, we hypothesized that it should also show sleep abnormalities relative to the control strain, the Wistar (WIS) rat Under baseline conditions, WKY rats showed a 50% increase in total REM sleep time during the 12 h light phase and an increase in sleep fragmentation during both the light and dark phase. The WKY rats also exhibited lower EEG power densities over the entire frequency range (0.2-25.0 Hz) during REM sleep. After a 6 h sleep deprivation, the REM sleep rebound was more pronounced during the dark but not the light phase in the WKY rats. Since the WKY rat represents a genetic model for depression with altered EEG sleep patterns, this strain may be particularly useful for investigating the relationship between depression and sleep abnormalities.

Animals↗
PubMed2000

[Melatonin. II. Physiological and therapeutic effects].

Melatonin is a hormone mainly secreted by the pineal gland during the dark phase of the light-dark cycle. The most known function of melatonin in mammals is to transmit information concerning light-dark cycles playing the role of an active neuroendocrine transducer of environmental information. Given this chronobiologic role of pineal melatonin, it seems to be useful in the management of shift work, jet lag and some sleep disorders. In vitro like in vivo melatonin seems to be effective as an antioxidant and oncostatic agent. Melatonin may provide protection against aging process, degenerative diseases, cancer and play a role also in sexual maturation, reproduction, immune function and psychiatric illness. The administration of melatonin in the jet-lag syndrome is well codified. Further clinical research is needed for a better understanding and definition of other indications, treatment regimens and safety of the hormone. The aim of this paper is to review the current knowledge on its clinical implications.

Anticarcinogenic Agents↗
PubMed1999

High corticosterone levels in prenatally stressed rats predict persistent paradoxical sleep alterations.

Prenatal stress predisposes rats to long-lasting disturbances that persist throughout adulthood (e.g., high anxiety, dysfunction of the hypothalamo-pituitary-adrenal axis, and abnormal circadian timing). These disturbances parallel to a large extent those found in depressed patients, in which hypercortisolemia and sleep alterations may be related to stress-inducing events. We studied sleep-wake parameters in control and prenatally stressed adult rats (3-4 months old) and examined possible relationships with their corticosterone levels (determined at 2 months of age). Under baseline conditions, prenatally stressed rats showed increased amounts of paradoxical sleep, positively correlated to plasma corticosterone levels. Other changes include increased sleep fragmentation, total light slow-wave sleep time, and a slight decrease in the percentage of deep slow-wave sleep relative to total sleep time. During recovery sleep from acute restraint stress, all sleep changes persisted and were correlated with stress-induced corticosterone secretion. High corticosterone levels under baseline conditions as well as an acute stress challenge may thus predict long-term sleep-wake alterations in rats. Taken together with other behavioral and hormonal abnormalities in prenatally stressed animals, the pronounced changes in sleep-wake parameters that are similar to those found in depressed patients suggest that prenatal stress may be a useful animal model of depression.

Analysis of Variance↗
PubMed1999

Prenatal stress alters circadian activity of hypothalamo-pituitary-adrenal axis and hippocampal corticosteroid receptors in adult rats of both gender.

Prenatal stress impairs activity of the hypothalamo-pituitary-adrenal (HPA) axis in response to stress in adult offspring. So far, very few data are available on the effects of prenatal stress on circadian functioning of the HPA axis. Here, we studied the effects of prenatal stress on the circadian rhythm of corticosterone secretion in male and female adult rats. To evaluate the effects of prenatal stress on various regulatory components of corticosterone secretion, we also assessed the diurnal fluctuation of adrenocorticotropin, total and free corticosterone levels, and hippocampal corticosteroid receptors. Finally, in the search of possible maternal factors, we studied the effects of repeated restraint stress on the pattern of corticosterone secretion in pregnant female rats. Results demonstrate that prenatal stress induced higher levels of total and free corticosterone secretion at the end of the light period in both males and females, and hypercorticism over the entire diurnal cycle in females. No diurnal fluctuation of adrenocorticotropin was observed in any group studied. The effects of prenatal stress on corticosterone secretion could be mediated, at least in part, by a reduction in corticosteroid receptors at specific times of day. Results also show that prepartal stress alters the pattern of corticosterone secretion in pregnant females. Those data indicate that prenatally stressed rats exhibit an altered temporal functioning of the HPA axis, which, taken together with their abnormal response to stress, reinforces the idea of a general homeostatic dysfunction in those animals.

Adrenocorticotropic Hormone↗
PubMed1999

A single oral dose of S 22153, a melatonin antagonist, blocks the phase advancing effects of melatonin in C3H mice.

Disorders of the circadian system have been associated with adverse mental and physical conditions, raising the possibility that pharmacological agents acting on the circadian system could have therapeutic benefit. Compounds acting as agonists or antagonists of melatonin, an endogenous hormone able to feed back on the circadian clock, are currently under development for possible use in modulating circadian rhythmicity. In the present study, we examined the ability of an oral dose of S 22153, a synthetic melatonin antagonist, to block the phase advancing effect of a melatonin injection at circadian time 10 in free running C3H mice. Our results show that S 22153 had no effect per se on the phase or the period of the locomotor activity rhythm but was able to block the phase advancing effect of melatonin, suggesting potent antagonist effects at melatonin receptors. Availability of a melatonin antagonist may yield new insight into the role of melatonin in physiological processes and such compounds may find widespread clinical applications.

Administration, Oral↗
PubMed1999

Chronobiotic effects of gepirone, a potential antidepressant with 5HT1A receptor partial agonist properties.

Abnormal timing in the circadian system is reported in endogenous depression. Gepirone, a 5HT1A receptor partial agonist, has anxiolytic and antidepressant properties. We determined whether gepirone was able to modify the functioning of the circadian system. Single i.p. injections of gepirone in hamsters induced phase-advances in the circadian activity rhythm when administered during the subjective day, but had no effect when given during the subjective night. Single i.p. gepirone injections also blocked the phase-shifting effects of a light pulse, at a time when gepirone by itself had no effect on the activity rhythm. Chronic gepirone treatment in hamsters kept under a 14/10 light-dark cycle induced a phase-advance in the activity rhythm, modifying the phase-relationship between this rhythm and the light-dark cycle. After transfer to constant darkness, gepirone-treated hamsters showed a shortened free-running period of activity, compared to controls. Both acute and chronic gepirone treatment thus have major effects on the circadian rhythm of locomotor activity in rodents. In view of the hypothesized role for disturbed circadian rhythms in the pathophysiology of depression, and the use of 5HT-related drugs for its treatment, the results provide further support for the possibility that some of the therapeutic effects of these compounds may be due to their effects on temporal organization.

Animals↗
PubMed1999

Pharmacologic and therapeutic features of sulbutiamine.

Asthenia is the most frequent medical reason for people seeking help from their physician. In 75% of cases, the cause is functional (either reactive or psychiatric) and in 25% it is organic. In order to provide patients with rapid relief of symptoms, appropriate antiasthenic treatment should be initiated immediately, while at the same time, adequate clinical and laboratory assessments should be performed to detect the underlying cause of asthenia. Sulbutiamine, a highly lipophilic thiamine derivative, is the only antiasthenic compound known to cross the blood-brain barrier and to be selectively active on specific brain structures directly involved in asthenia. This article reviews the current knowledge on the effects of sulbutiamine in animal models and in various forms of human asthenia.

Journal Article↗
PubMed1998

Resynchronisation of a diurnal rodent circadian clock accelerated by a melatonin agonist.

Using 'jet lag' paradigms involving phase shifts in the light-dark (LD) cycle, we studied the effects of S-20098 on the circadian clock of a diurnal rodent. Arvicanthis mordax, entrained to a regular LD cycle, were subjected to advance shifts (i.e. 4, 6 or 8 h) in the LD cycle and injected with vehicle or the melatonin agonist S-20098 (20 mg/kg) the day of the shift (and also on subsequent days in the 6 h or 8 h shift paradigms). In each condition, S-20098 accelerated by about 30% resynchronization to the new LD cycle. These data, which are the first to demonstrate the chronobiotic effects of a melatonin agonist in a diurnal rodent, provide new insights for the design of human chronopharmacological protocols.

Acetamides↗
PubMed1998

Effects of exercise on neuroendocrine secretions and glucose regulation at different times of day.

To study the effects of time of day on neuroendocrine and metabolic responses to exercise, body temperature, plasma glucose, insulin secretion rates (ISR), and plasma cortisol, growth hormone (GH) and thyrotropin (TSH) were measured in young men, both at bed rest and during a 3-h exercise period (40-60% maximal O2 uptake). Exercise was performed at three times of day characterized by marked differences in cortisol levels, i.e., early morning (n = 5), afternoon (n = 8), and around midnight (n = 9). The subjects were kept awake and fasted, but they received a constant glucose infusion to avoid hypoglycemia. Exercise-induced elevations of temperature were higher in the early morning than at other times of day. The exercise-induced glucose decrease was approximately 50% greater around midnight, when cortisol was minimal and not stimulated by exercise, than in the afternoon or early morning (P < 0.05). This effect of time of day appeared unrelated to decreases in ISR or increases in temperature and GH. Robust TSH increases occurred in all exercise periods and were maximal at night. The results demonstrate the existence of circadian variations in neuroendocrine and metabolic responses to exercise.

Adult↗
PubMed1998

Sleep and circadian disturbances in shift work: strategies for their management.

More and more businesses are providing their full range of services 24 h a day, 7 days a week, thus forcing their employees to work either rotating shifts or fixed night shifts. Dictates of our endogenous circadian clock prevent our brains and bodies to be indefinitely adaptable to those work schedules. Shift work operations are thus associated with serious healthy and social problems for the workers. Various interventions can counteract circadian desynchronization, sleep disturbances, and social disruption associated with shift work: changes in work schedules, sleeping and napping strategies, use of appropriately timed exposure to bright light, experimental drug treatments, or exercise.

Adaptation, Psychological↗