PubMed Health⌕ Search

Biomedical subjects

D Davenne

Publications and source records attributed to D Davenne.

At least 19 recordsLinked to original sources
PubMed1992

Met-enkephalin, beta-endorphin and cortisol responses to sub-maximal exercise after sleep disturbances.

The present study compared the effects of partial sleep deprivation and the effects of an intake of a hypnotic compound (zolpidem) prior to bedtime, on sleep and on hormonal and metabolic adaptations to subsequent exercise. Sleep deprivation consisted of a delayed bedtime and an early getting-up time. Eight young subjects, who slept well and were highly trained athletes, were enrolled in this study. Sleep was recorded polygraphically and the following afternoon exercise was performed on a cycle ergometer for 30 min at 75% of maximal oxygen consumption (VO2max) after a 10-min warm up. Met-enkephalin, beta-endorphin, cortisol, and lactate concentrations were measured at rest and during exercise. The data obtained after experimental sleep, with and without medication were compared with those obtained in the reference condition with normal sleep. Both types of sleep reduction decreased the total sleep time, stage 2 sleep, and rapid eye movement sleep, whereas zolpidem administration did not modify either the duration of sleep or the sleep stages. After the reference night, plasma met-enkephalin did not show any significant change at the end of the submaximal exercise, whereas beta-endorphin, cortisol, and lactic acid concentrations increased significantly in all subjects. The changes in concentration in beta-endorphin were significantly related to the changes in cortisol (r = 0.78; P less than 0.01) and to the changes in plasma lactic acid (r = 0.58; P less than 0.05). Cortisol concentrations were also related to lactic acid values (r = 0.94; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of sleep disturbances on subsequent physical performance.

The purpose of the study was to compare the cardiovascular, respiratory and metabolic responses to exercise of highly endurance trained subjects after 3 different nights i.e. a baseline night, a partial sleep deprivation of 3 h in the middle of the night and a 0.25-mg triazolam-induced sleep. Sleep-waking chronobiology and endurance performance capacity were taken into account in the choice of the subjects. Seven subjects exercised on a cycle ergometer for a 10-min warm-up, then for 20 min at a steady exercise intensity (equal to the intensity corresponding to 75% of the predetermined maximal oxygen consumption) followed by an increased intensity until exhaustion. The night with 3 h sleep loss was accompanied by a greater number of periods of wakefulness (P less than 0.01) and fewer periods of stage 2 sleep (P less than 0.05) compared with the results recorded during the baseline night. Triazolam-induced sleep led to an increase in stage 2 sleep (P less than 0.05), a decrease in wakefulness (P less than 0.05) and in stage 3 sleep (P less than 0.05). After partial sleep deprivation, there were statistically significant increases in heart rate (P less than 0.05) and ventilation (P less than 0.05) at submaximal exercise compared with results obtained after the baseline night. Both variables were also significantly enhanced at maximal exercise, while the peak oxygen consumption (VO2) dropped (P less than 0.05) even though the maximal sustained exercise intensity was not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Regulation of noradrenergic coerulean neuronal firing mediated by 5-HT2 receptors: involvement of the prepositus hypoglossal nucleus.

Previous studies have indicated a 5-HT2-mediated inhibitory influence on unit activity in the locus coeruleus. In the present work, attempts were made to determine which area(s) of the brain is (are) involved in this effect: (1) Microiontophoretic application of serotoninergic compounds (quipazine, ketanserin, RU 24969 (Roussel Uclaf), 8-hydroxy-2(di-n-propylamino) tetralin (8-OH-DPAT), metergoline, serotonin) in the locus coeruleus, did not alter the coerulean discharge. Local microinjection of quipazine or ketanserin in the area of the locus coeruleus, as well as in one of its major afferents, the prepositus hypoglossi, had no effect on the unit activity in the locus coeruleus. (2) Section of the forebrain, caudal to the frontal cortex (rich in 5-HT2 receptors), did not modify the effects of coerulean activity of quipazine-ketanserin injected systemically: quipazine induced an inhibition which was reversed by ketanserin. In contrast, these effects were significantly reduced after the bilateral or contralateral lesion of the prepositus hypoglossi. It is concluded that the prepositus hypoglossal nucleus is part of the network responsible for the 5-HT2-mediated control of unit activity in the locus coeruleus.

Animals↗
PubMed1989

Lesion of the PGO pathways in the kitten. II. Impairment of physiological and morphological maturation of the lateral geniculate nucleus.

Suppression of the geniculate ponto-geniculo-occipital (PGO) waves by bilateral lesions of PGO pathways at the mesencephalic level in 15-day-old kittens has been shown to induce a significant reduction of the mean discharge frequency recorded in the lateral geniculate nucleus (LGN) during paradoxical sleep. The present paper reports that one month after the bilateral lesion (i.e., 6-7 weeks of age) important deficits in the maturation of the LGN were observed: (1) electrophysiologically, the latencies of the LGN cellular responses to stimulation of the optic chiasm were significantly longer than those of age-paired controls or of unilaterally lesioned animals, and the proportion of visual cells characterized as type X by stimulation of the visual field was smaller; and (2) morphologically, the volume of the LGN and the size of its neuronal somata were smaller than those in control. These data suggest that bilateral suppression of extraretinal PGO afferents to the LGN in the kitten induces a significant delay in the development of this nucleus.

Action Potentials↗
PubMed1989

[Current physiologic data on sleep].

Sleep is organized as a succession of different physiological states. Despite the fact that the mechanisms which regulate these states has been located in the central nervous system, our knowledge of these regulations is very poor. In this paper, different hypothesis implying brain locations, neurotransmitters, and neuroimmunomodulators are shortly described.

Age Factors↗
PubMed1989

[Disturbance of sports performance after partial sleep deprivation].

The changes in cardiac and ventilatory responses were measured in 7 endurance athletes during physical exercise on a bicycle ergometer, taking place after a control night and after a night with partial sleep deprivation in the middle of the night. The results show that, despite the maximal work load was not modified with control, heart rate, ventilation and VE/VO2 ratio (ERO2) were greater at the submaximal (75% of the VO2 max) and maximal work load and oxygen consumption decreased at maximal work, after the night of partial sleep deprivation as compared to the control. These findings suggest that acute sleep loss may contribute to alter the endurance performance by impairment of aerobic pathways.

Adult↗
PubMed1987

Lesion of the ponto-geniculo-occipital pathways in kittens. I. Effects on sleep and on unitary discharge of the lateral geniculate nucleus.

Suppression of geniculate ponto-geniculo-occipital (PGO) waves was achieved in kittens by performing bilateral mesencephalic lesions of the PGO pathways. Sleep-wake parameters and the spontaneous unit activity in the lateral geniculate nucleus (LGN) were then chronically recorded during one month after the lesions. Whereas the states of vigilance remained normal, a significant reduction of the unitary discharge in the LGN during paradoxical sleep (PS) and particularly of its phasic component, was observed concomitantly with the suppression of PGO waves. It is concluded that phasic discharge of LGN neurons during PS is controlled by PGO-related mechanisms and that its suppression during the developmental period provides a model for studying its significance on brain maturation.

Animals↗
PubMed1987

Bacterial peptidoglycans as modulators of sleep. I. Anhydro forms of muramyl peptides enhance somnogenic potency.

Chemically defined muramyl peptides (MPs), derived primarily from enzymatic digests of Neisseria gonorrhoeae peptidoglycan, were used to define the structural determinants of MP-mediated somnogenic activity. One of these, i.e. N-acetylglucosaminyl-N-acetyl-1,6-anhydro-N-acetylmuramyl-alanyl-glutamy l- diaminopimelyl-alanine, was structurally identical to the major naturally occurring MP previously detected in mammalian brain and urine. The somnogenic potency of this MP was similar to that of the corresponding disaccharide pentapeptide containing an additional alanine at the C-terminus and the analogous anhydro-muramic acid-containing monosaccharide tetrapeptide lacking the glucosamine moiety. Infusion of as little as 1 pmol of these highly active MPs increased significantly the percentage of slow-wave sleep in experimental animals. In fact, each of 5 anhydro-muramyl disaccharide peptides tested was somnogenic at a dose of 10 pmol or less and, as far as tested, the activity was affected only slightly by the length or composition of the peptide side chain. However, none of a matched set of analogous MPs, differing only in replacement of the anhydro-muramyl end by a hydrated muramic acid residue, was somnogenic at this dose. A modified form of the hydrated muramyl tripeptide containing a free amide on the diaminopimelic acid residue was completely inactive in amounts up to 1000 pmol. Together, the current data suggested: that the anhydro-muramic acid end (but not the glucosamine moiety) is essential for maximal somnogenic potency; and that amidation of carboxyl groups on the peptide-side chain may block MP-mediated somnogenic activity.

Anhydrides↗
PubMed1987

Bacterial peptidoglycans as modulators of sleep. II. Effects of muramyl peptides on the structure of rabbit sleep.

Sleep-promoting substances derived from human urine and rabbit brain were identified as muramyl peptides (MPs). We report in the accompanying paper that in the molecular structure of MPs, the 1,6-anhydro muramic acid moiety of MPs is important for enhancement of slow-wave sleep (SWS) in rabbits. Here, we document more extensively the effects of one MP: 1,6-anhydro-muramyl-alanyl-glutamyl-diaminopimelyl-alanine (AMTP for anhydro-muramyl tetrapeptide) on sleep structure of rabbits. AMTP significantly increased percent of time spent in SWS but its effects on rapid eye movement (REM) sleep were dose-dependent. Brain temperatures were significantly elevated but continued to fluctuate with sleep and wake state transitions indistinguishably from control. Sleep was episodic and animals could be easily aroused. AMTP increased number of SWS episodes and decreased number of REM episodes. There was a shift in the distribution of sleep-wake episode durations: longer waking and REM episodes were decreased, thus increased the proportion of shorter episodes. Increased duration of SWS resulted from a larger number of SWS episodes longer than 8 min. We conclude that AMTP amplifies the SWS compenent of physiological sleep.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1987

Muramyl dipeptide, amphetamine, and physostigmine: effects on sleep of rabbits.

Muramyl peptides (MPs) are constituents of bacterial cell walls and mammalian tissue. Some MPs have the capacity to enhance slow-wave sleep (SWS). In rabbits, it was unknown whether MPs enhanced SWS by prolonging SWS episodes or by increasing the number of SWS episodes. In rabbits, there is a frequent alternation between sleep and waking; thus, demonstration of induction of new SWS episodes is difficult unless pharmacologic manipulations are used. We injected amphetamine subcutaneously to reduce duration of sleep (from about 45% to 20%) for a period of two hours; it reduced the number of SWS episodes. Muramyl dipeptide (MDP: NAM-L-ala-D-isogln) injected into a lateral ventricle one hour before amphetamine significantly increased the number of SWS episodes. Physostigmine, a cholinergic agonist, was also used. By itself, physostigmine greatly reduced SWS and rapid eye movement sleep. Pretreatment of animals with MDP two hours before physostigmine injection failed to reverse subsequent physostigmine-induced wakefulness. We conclude that MDP has the ability to induce SWS episodes but does not act directly on the thalamocortical cholinergic mechanisms of EEG phenomena. Our results, together with earlier evidence on anatomical levels of action of amphetamine and physostigmine, suggest that the somnogenic mechanisms of MPs likely involve the midbrain.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1987

Interferon alpha-2 enhances slow-wave sleep in rabbits.

Interferon alpha-2 (IFN) is a leukocyte product with several biological properties including antiviral activity, pyrogenicity and enhancement of immune functions. We report here that an additional facet of IFN activity is its ability to enhance slow-wave sleep (SWS) without greatly altering other aspects of sleep. Intravenous or cerebral intraventricular injections of human IFN into rabbits induced enhancement of SWS, electroencephalographic slow-wave (0.5-4 Hz) activity and brain temperatures. IFN induced slight reductions in rapid-eye movement sleep. Animal behavior, brain temperature changes that occur during the transition from one arousal state to another, and the cyclic nature of states of vigilance remained undisturbed after IFN treatment. The sleep-promoting activity of IFN may be related to feelings of lassitude and sleepiness that often accompany viral disease and interferon therapy. That IFN and other immunoactive substances, e.g. interleukin-1 and muramyl peptides, can enhance sleep suggests that sleep is linked into the immune response.

Animals↗
PubMed1987

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

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.

Animals↗
PubMed1987

Enhancement of quiet sleep in rabbit neonates by muramyl dipeptide.

Muramyl peptides that induce excess slow-wave sleep have been isolated from urine and brain. A synthetic analogue to those substances, muramyl dipeptide (MDP, N-acetylmuramyl-L-alanyl-D-isoglutamine), was found to induce prolonged increases in slow-wave sleep and to increase electroencephalographic (EEG) delta-wave activity. MDP is also pyrogenic, although this activity can be separated from its somnogenic activity. To further investigate the somnogenic actions of MDP, neonatal rabbits were used in the present study. Intraperitoneal injection of 100 micrograms/kg MDP induced differential somnogenic and pyrogenic effects; from postnatal days 7-9, MDP increased duration of quiet sleep (QS, the precursor of adult slow-wave sleep) and decreased active sleep (AS) as judged by behavioral criteria. These animals were not febrile during the period of enhanced QS, nor did MDP alter EEG delta-wave activity at this age. From postnatal days 10-15, MDP induced prolonged (6 h) increases in duration of QS; both behavioral and EEG criteria were used at this age to determine duration of QS and AS. Maximum MDP-induced effects occurred during the 2nd h, with a parallel increase in amplitudes of EEG delta-wave activity. At this age, MDP also elicited monophasic fevers and inhibition of AS, with maximum effects observed during hours 3-4 postinjection. After postnatal day 16, MDP-induced somnogenic and febrile responses were similar to those observed in adult rabbits. We conclude that the mechanisms responsible for behavioral sleep states are responsive to a sleep-promoting substance early in ontogenesis.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1986

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

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.

Animals↗
PubMed1986

Enhancement of slow-wave sleep by endotoxin and lipid A.

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.

Animals↗
PubMed1986

Somnogenic muramyl peptides.

Sleep-promoting materials isolated from human urine and rabbit brain are muramyl peptides (MPs). The most active component of the urinary material is N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-Ala-Glu-diaminopimel yl-Ala; 1 pmol, infused into a lateral cerebral ventricle of rabbits, induced excess slow-wave sleep (SWS) for several hours. MP-induced sleep is normal in that it is similar to the deep sleep that follows sleep deprivation. Other biological actions of MPs (e.g., pyrogenicity and immunomodulatory activity) could be dissociated, but only in part, from somnogenic actions. Interleukin 1, a substance thought to mediate many MP activities, is somnogenic, and thus may be involved in MP-induced sleep. That MPs and other immunologically active substances can greatly enhance SWS suggests that some immunological mechanisms integrate sleep in their actions.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

[Electrophysiological maturation of neurons of the lateral geniculate nucleus after lesion of ponto-geniculo-occipital pathways in kittens].

Bilateral mesencephalic lesions, which suppress the PGO activity in the lateral geniculate nucleus (LGN), were performed at two weeks of age in the kitten, and the effects on the electrophysiological development of this nucleus were analyzed at 6 weeks of age. The latencies of LGN cells after electrical stimulation of the optic chiasma were larger, and the number of the differentiated X cells was smaller than those of age paired controls. However, the response of the ganglion fibers was not modified. These results, compared to those obtained on 30 days old kittens, and on animals with a unilateral lesion, suggest that the suppression of PGO inputs to the LGN induced a delay in the electrophysiological maturation of this nucleus.

Animals↗