Home About us Contact
|
Home About us Contact | ||
|
|
||
Non-rapid Eye Movement Sleep (non-rapid + eye_movement_sleep)
Selected AbstractsHippocampal adult neurogenesis is enhanced by chronic eszopiclone treatment in ratsJOURNAL OF SLEEP RESEARCH, Issue 3 2010MELVI METHIPPARA Summary The adult hippocampal dentate gyrus (DG) exhibits cell proliferation and neurogenesis throughout life. We examined the effects of daily administration of eszopiclone (Esz), a commonly used hypnotic drug and ,-aminobutyric acid (GABA) agonist, compared with vehicle, on DG cell proliferation and neurogenesis, and on sleep,wake patterns. Esz was administered during the usual sleep period of rats, to mimic typical use in humans. Esz treatment for 7 days did not affect the rate of cell proliferation, as measured by 5-bromo-2,-deoxyuridine (BrdU) immunostaining. However, twice-daily Esz administration for 2 weeks increased survival of newborn cells by 46%. Most surviving cells exhibited a neuronal phenotype, identified as BrdU,neuronal nuclei (NeuN) double-labeling. NeuN is a marker of neurons. Non-rapid eye movement sleep was increased on day 1, but not on days 7 or 14 of Esz administration. Delta electroencephalogram activity was increased on days 1 and 7 of treatment, but not on day 14. There is evidence that enhancement of DG neurogenesis is a critical component of the effects of antidepressant treatments of major depressive disorder (MDD). Adult-born DG cells are responsive to GABAergic stimulation, which promotes cell maturation. The present study suggests that Esz, presumably acting as a GABA agonist, has pro-neurogenic effects in the adult DG. This result is consistent with evidence that Esz enhances the antidepressant treatment response of patients with MDD with insomnia. [source] Sleep and Rest Regulation in Young and Old Oestrogen-Deficient Female MiceJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006V. V. Vyazovskiy The effect of circulating oestrogen deficiency on sleep regulation and locomotor activity was investigated in aromatase cytochrome P450 deficient mice (ArKO) and wild-type (WT) controls. Sleep was recorded in 3-month old mice during a 24-h baseline day, 6-h sleep deprivation (SD) and 18-h recovery, and activity was recorded at the age of 3, 9 and 12 months. In mice deficient of oestrogen, the total amount of sleep per 24 h was the same as in WT controls. However, in ArKO mice, sleep was enhanced in the dark period at the expense of sleep in the light phase, and was more fragmented than sleep in WT mice. This redistribution of sleep resulted in a damped amplitude of slow-wave activity (SWA; power between 0.75,4.0 Hz) in non-rapid eye movement sleep across 24 h. After SD, the rebound of sleep and SWA was similar between the genotypes, suggesting that oestrogen deficiency does not affect the mechanisms maintaining the homeostatic balance between the amount of sleep and its intensity. Motor activity decreased with age in both genotypes and was lower in ArKO mice compared to WT at all three ages. After SD, the amount of rest in 3-month old WT mice increased above baseline and was more consolidated. Both effects were less pronounced in ArKO mice, reflecting the baseline differences between the genotypes. The results indicate that despite the pronounced redistribution of sleep and motor activity in oestrogen deficient mice, the basic homeostatic mechanisms of sleep regulation in ArKO mice remain intact. [source] Long-term vs. short-term processes regulating REM sleepJOURNAL OF SLEEP RESEARCH, Issue 1 2002PAUL FRANKEN In cats, rats, and mice, the amount of rapid eye movement sleep (REMS) lost during a sleep deprivation (SD) predicts the subsequent REMS rebound during recovery sleep. This suggests that REMS is homeostatically regulated and that a need or pressure for REMS accumulates in its absence, i.e. during both wakefulness and non-rapid eye movement sleep (NREMS). Conversely, it has been proposed that REMS pressure accumulates exclusively during NREMS [Benington and Heller, Am. J. Physiol. 266 (1994) R1992; Prog. Neurobiol. 44 (1994b) 433]. This hypothesis is based on the analysis of the duration of successive NREMS and REMS episodes and of electroencephalogram (EEG) events preceding REMS. Pre-REMS events (PREs) do not always result in sustained REMS and can thus be regarded as REMS attempts that increase as NREMS progresses. It is assumed that two processes regulating REMS can resolve the apparent contradiction between these two concepts: a `long-term' process that homeostatically regulates the daily REMS amount and a `short-term' process that regulates the NREM,REMS cycle. These issues were addressed in two SD experiments in rats. The two SDs varied in length (12 and 24 h) and resulted in very similar compensatory changes in NREMS but evoked very different changes for all REMS parameters studied. The large REMS increase observed after 24-h SD was accompanied by a reduction in unsuccessful PREs and an increase in sustained REMS episodes, together resulting in a threefold increase in the success-rate to enter REMS. Changes in success-rate matched those of a theoretically derived long-term REMS pressure. The SD induced changes in sleep architecture could be reproduced by assuming that the increased long-term REMS pressure interacts with the short-term process by increasing the probability to enter and remain in REMS. [source] Optimization of sigma amplitude threshold in sleep spindle detectionJOURNAL OF SLEEP RESEARCH, Issue 4 2000E. Huupponen Sleep spindles are transient EEG waveforms of non-rapid eye movement sleep. There is considerable intersubject variability in spindle amplitudes. The problem in automatic spindle detection has been that, despite this fact, a fixed amplitude threshold has been used. Selection of the spindle detection threshold value is critical with respect to the sensitivity of spindle detection. In this study a method was developed to estimate the optimal recording-specific threshold value for each all-night recording without any visual scorings. The performance of the proposed method was validated using four test recordings each having a very different number of visually scored spindles. The optimal threshold values for the test recordings could be estimated well. The presented method seems very promising in providing information about sleep spindle amplitudes of individual all-night recordings. [source] Severe obstructive sleep apnea: Sleepy versus nonsleepy patientsTHE LARYNGOSCOPE, Issue 3 2010Arie Oksenberg PhD Abstract Objectives/Hypothesis: To compare demographic and polysomnographic data of sleepy versus nonsleepy severe obstructive sleep apnea (OSA) patients according to the Epworth Sleepiness Scale (ESS). Study Design: Retrospective cohort. Methods: Six hundred forty-four consecutive severe (apnea-hypopnea index [AHI] , 30) adult OSA patients who underwent a polysomnographic evaluation in our sleep disorders unit. ESS data were available in 569 (88.3%). Three hundred twenty-seven (57.5%) patients had ESS > 10. Results: Sleepy severe OSA patients are slightly younger and more obese than nonsleepy patients. These sleepy patients have shorter sleep latency and lower percentage of slow wave sleep. They consistently show a higher AHI, both supine and lateral AHI, have a higher number of short arousals, and a higher arousal index. They also have higher snoring loudness in the supine and both lateral positions and a lower minimal SaO2 in rapid eye movement and non-rapid eye movement sleep. After adjusting for confounders, a logistic regression model points to apnea index as a significant prognostic factor for excessive daytime sleepiness. Conclusions: Severe OSA sleepy patients have a syndrome that is significantly more severe than nonsleepy patients. Sleepy patients have worse sleep-related breathing parameters, and their sleep patterns are lighter and more fragmented than nonsleepy patients. Apnea index appears as an important prognostic factor for excessive daytime sleepiness. Laryngoscope, 2010 [source] Sleep induced by stimulation in the human pedunculopontine nucleus areaANNALS OF NEUROLOGY, Issue 4 2010Isabelle Arnulf MD The pedunculopontine nucleus is part of the reticular ascending arousal system and is involved in locomotion and sleep. Two patients with Parkinson disease received electrodes that stimulated the pedunculopontine nucleus area to alleviate their severe gait impairment. Instead, we found that low-frequency stimulation of the pedunculopontine nucleus area increased alertness, whereas high-frequency stimulation induced non-rapid eye movement sleep. In addition, the sudden withdrawal of the low-frequency stimulation was consistently followed by rapid eye movement sleep episodes in 1 patient. These data have the potential to benefit patients who suffer from sleep disorders. ANN NEUROL 2010;67:546,549 [source] PHYSIOLOGICAL SLEEP-DEPENDENT CHANGES IN ARTERIAL BLOOD PRESSURE: CENTRAL AUTONOMIC COMMANDS AND BAROREFLEX CONTROLCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2008Alessandro Silvani SUMMARY 1Sleep is a heterogeneous behaviour. As a first approximation, it is subdivided objectively into two states: non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). 2The mean value and variability of arterial blood pressure (ABP) decrease physiologically from wakefulness to NREMS. In REMS, there may be a further decrease or increase in mean ABP as well as phasic hypertensive events, which enhance the variability of ABP. 3The reduced mean ABP during NREMS results from a decrease in either heart rate or sympathetic vasoconstrictor tone. During REMS, sympathetic activity to the different cardiovascular effectors undergoes a substantial repatterning. Thus, the mean ABP in REMS reflects a balance between changes in cardiac output and constriction or dilatation of different vascular beds. 4In both sleep states, the phasic changes in ABP are driven by bursts of vasoconstriction, which may be accompanied by surges of heart rate. 5The available evidence supports the hypothesis that the sleep-dependent changes in ABP, either tonic or phasic, result from the integration between cardiovascular reflexes and central autonomic commands that are specific to each sleep state. [source] | ||||||||||