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1
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Event-related desynchronization and synchronization in evoked K-complexes

100%
Zygierewicz J., Malinowska U., Suffczynski P., Piotrowski T., Durka P. J.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 2
254-26
EN
K-complexes ? phenomena occurring in sleep EEG ? pose severe challenges in terms of detection as well as finding their physiological origin. In this study, K-complexes (KCs) were evoked by auditory stimuli delivered during sleep. The use of evoked KCs enables testing the sleeping nervous system under good experimental control. This paradigm allowed us to adopt into the KC studies a method of signal analysis that provides time-frequency maps of statistically significant changes in signal energy density. Our results indicate that KCs and sleep spindles may be organized by a slow oscillation. Accordingly, KCs might be evoked only if the stimulus occurs in a certain phase of the slow oscillation. We also observed middle-latency evoked responses following auditory stimulation in the last sleep cycle. This effect was revealed only by the time-frequency maps and was not visible in standard averages.
2
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Analysis of complexity of EEG during sleep

100%
Szelenberger W., Wackerman J., Skalski M., Niemcewicz S., Drojewski J.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
165-169
EN
New multichannel descriptors of EEG activity: complexity (Omega), total power (Sigma) and generalized frequency (Phi) were applied to whole night sleep analysis in 11 healthy subjects. The values of Omega and Phi decreased systematically from waking to slow wave sleep, and increased systematically in consecutive NREM-REM sleep cycles. The changes of Sigma were opposite to Omega and Phi. These descriptors may be an alternative approach to the EEG sleep analysis.
3
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The modified Color Density Spectral Array - an alternative method for sleep presentation

100%
Pracki T., Pracka D., Ziolkowska-Kochan M., Tafll-Klawe M., Szota A., Wilkosc M.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 4
516-518
EN
patterns is described in this article. CDSA was presented for the first time in 1987 by M. Salinsky and coauthors. This method was adapted to display frequency course and voltage of EEG signal during sleep. The overnight sleep records of 35 healthy volunteers of both sexes (23 women, 12 men; aged 1926) were analyzed in order to verify the modification of CDSA method. We propose to use combining the hypnogram and CDSA method significantly increases the informative value of data and results in enhanced quality of sleep analysis.
4
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Differential effects of non-REM and REM sleep on sensory gating in rats

80%
van_ L. E. L., Miller C. A. F. J., Coenen A. M. L., Drinkenburg W. H. I. M., Ellenbroek B. A.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
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issue 4
263-270
EN
Sensory gating in rats can be measured with a double click paradigm. The diminished response towards the second click is a physiological manifestation of reduced sensory input. This physiological process seems to be disturbed in human psychoses. It is thought that gating, as measured with this paradigm, is a preattentive, involuntary phenomenon which is not modulated by attention. If this is indeed the case, than it is hypothesized that gating should not be modulated by non-REM sleep. In the present experiment pairs of clicks (500 ms interval) were presented during wakefulness, non-REM as well as REM sleep and cortical auditory evoked potentials (AEP's) were recorded in chronically implanted rats. Rather similar AEP's were found after the first and second stimulus. However, the amplitudes of the various components of the second AEP were smaller than those of the first AEP, suggesting a gated response. This was the case during all three levels of vigilance. The amplitudes of both AEP's showed the more often reported changes in amplitude during sleep and REM sleep. Clear differences were seen in gating: compared to wakefulness a decrease in gating was found during REM sleep while gating was unchanged during non-REM sleep. The latter outcome seems to confirm that gating in rats is indeed a preattentive process. Finally, results were discussed in terms of neuronal properties of thalamic relay cells and it is suggested that firing properties of thalamic relay cells are not involved in this type of sensory gating.
5
Content available remote

Interhemispheric differences of sleep EEG complexity

80%
Szelenberger W., Wackermann J., Skalski M., Drojewski J., Niemcewicz S.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 4
955-959
EN
Complexity of EEG (W), a global measure reflecting degree of spatial synchronization, was computed for whole night recordings of sleep EEG of 10 healthy volunteers, 9 males and 1 female (age 21-53) and 6 depressive patients, 5 males and 1 female (age 23-64). Sleep was scored visually in 20's epochs, W was calculated in 2.5 s segments and the median from 8 segments (20 s) was calculated. W was calculated for the whole field of 21 electrodes and for the left and right hemisphere separately (2 x 8 electrodes). Measure of global power (S) and generalized frequency (f) were also computed for the same data. In healthy subjects the complexity was higher over the right hemisphere during waking, and the difference shifted to higher complexity over the left hemisphere in slow wave sleep (F=5.15, df1=4, df2=6856, P<0.0005). The opposite trend was found in depressives (F=10.51, dfl=4, df2=3960, P<0.0001).
6
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Visceral signals reach visual cortex during slow wave sleep. Study in monkeys

70%
Pigarev I., Almirall H., Pigareva M. L., Bautista V., Sanchez-Bahillo A., Barcia C., Trinidad H. M.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 1
69-73
EN
Propagation of signals from the gastro-intestinal system towards the occipital cortex within sleep-wake cycle was investigated in three monkeys used in the study of sleep impairment in a chronic MPTP model of Parkinsonism. The monkeys differed in motor abilities and sleep structure. One animal (M1) was non-motor disabled and had no sleep alterations. The other two monkeys were severely motor affected, but one (M2) had normal sleep cycles; meanwhile, the other (M3) had no complete sleep cycles. To evaluate the level of sleep and to record cortical evoked responses screw electrodes were implanted over the occipital cortex. Two hours before overnight recordings, two hook electrodes were injected intraperitoneally (under light Ketanest anesthesia) and anchored in gut. Using these electrodes, electric stimulation was applied during slow wave sleep, and in wakefulness. Cortical evoked responses to intraperitoneal stimulation were found indeed during sleep in experiments with M1 and M2. These results show that also in primates with normal sleep pattern visceral information is transferred to the cerebral cortex during slow wave sleep.
7
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Cortical evoked responses to magnetic stimulation of macaque's abdominal wall in sleep-wake cycle

70%
Pigarev I. N., Almirall H., Pigareva M. L.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 1
91-96
EN
EEG and eye movements (magnetic search coil method) were recorded in sleep and wakefulness in a monkey (Macaca fascicularis) while the animal was sitting in a primate chair. Single pulse magnetic stimulation was applied to the monkey's abdominal wall using a circular coil and a Magstim 200 stimulator. Magnetic stimuli did not wake the sleeping animal, and being applied during slow wave sleep evoked clear responses in EEG with a latency of 80?100 ms. These responses disappeared during wakefulness and rapid eye movement sleep. Control experiments confirmed that these responses were not caused by the acoustic clicks produced by the magnetic coil. Results of this study further confirm that during sleep, signals from visceral organs reach the cortical areas which in wakefulness process exteroceptive sensory information. This observation indicates that magnetic stimulation may be a useful tool for researching neural connectivity reorganization within the sleep-wake cycle.
8
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Brain preconditioning and obstructive sleep APNEA syndrome

70%
Brzecka A.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
213-220
EN
Intermittent hypoxia stimulates the development of adaptive responses, called preconditioning. This process is partially mediated by genetic remodeling, via hypoxia inducible factor (HIF), which induces long-term adaptation processes and is responsible for the increase of levels of vascular endothelial growth factor (VEGF), erythropoietin (Epo), atrial natriuretic peptide (ANP), and nitric oxide (NO). The synthesis of brain-derived neurotrophic factor (BDNF) participates in the control of neural plasticity after hypoxia. The mechanisms of neuroprotection against hypoxia may be related to vascular adjustments and to central neurogenic neuroprotection. Some of the factors known to be involved in the development of the mechanism of neuroprotection are also present in the responses to repetitive apneas that occur during sleep in patients with obstructive sleep apnea (OSA) syndrome, who are frequently exposed to severe sleep hypoxemia. It appears that OSA syndrome represents a clinical example of preconditioning and the development of adaptive responses to intermittent hypoxia.
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