Biomedical subjects

Roland Dürr

Publications and source records attributed to Roland Dürr.

4 recordsLinked to original sources

PubMed2006

Adenosinergic mechanisms contribute to individual differences in sleep deprivation-induced changes in neurobehavioral function and brain rhythmic activity.

Large individual differences characterize the changes induced by sleep deprivation on neurobehavioral functions and rhythmic brain activity. To investigate adenosinergic mechanisms in these differences, we studied the effects of prolonged waking and the adenosine receptor antagonist caffeine on sustained vigilant attention and regional electroencephalogram (EEG) power in the ranges of theta activity (6.25-8.25 Hz) in waking and the slow oscillation (<1 Hz) in sleep. Activity in these frequencies is functionally related to sleep deprivation. In 12 subjectively caffeine-sensitive and 10 -insensitive young men, psychomotor vigilance task (PVT) performance and EEG were assessed at 3 h intervals before, during, and after one night without sleep. After 11 and 23 h waking, subjects received 200 mg caffeine and placebo in double-blind, cross-over manner. In the placebo condition, sleep deprivation impaired PVT speed more in caffeine-sensitive than in caffeine-insensitive men. This difference was counteracted by caffeine. Theta power in waking increased more in a frontal EEG derivation than in a posterior derivation. Caffeine attenuated this power gradient in caffeine sensitive subjects. Sleep loss also differently affected the power distribution <1 Hz in non-rapid eye movement sleep between caffeine sensitive and insensitive subjects. Also, this difference was mirrored by the action of caffeine. The effects of sleep deprivation and caffeine on sustained attention and regional EEG power in waking and sleep were inversely related. These findings suggest that adenosinergic mechanisms contribute to individual differences in waking-induced impairment of neurobehavioral performance and functional aspects of EEG topography associated with sleep deprivation.

Adenosine↗

PubMed2006

Sleep deprivation impairs object recognition in mice.

Many studies in animals and humans suggest that sleep facilitates learning, memory consolidation, and retrieval. Moreover, sleep deprivation (SD) incurred after learning, impaired memory in humans, mice, rats, and hamsters. We investigated the importance of sleep and its timing in an object recognition task in OF1 mice subjected to 6h SD either immediately after the acquisition phase (0-6 SD) or 6h later (7-12 SD), and in corresponding undisturbed controls. Motor activity was continuously recorded with infrared sensors. All groups explored two familiar, previously encountered objects to a similar extent, both at the end of the acquisition phase and 24h later during the test phase, indicating intact familiarity detection. During the test phase 0-6 SD mice failed to discriminate between the single novel and the two familiar objects. In contrast, the 7-12 SD group and the two control groups explored the novel object significantly longer than the two familiar objects. Plasma corticosterone levels determined after SD did not differ from time-matched undisturbed controls, but were significantly below the level measured after learning alone. ACTH did not differ between the groups. Therefore, it is unlikely that stress contributed to the memory impairment. We conclude that the loss of sleep and the activities the mice engaged in during the SD, impaired recognition memory retrieval, when they occurred immediately after acquisition. The delayed SD enabled memory consolidation during the 6h when the mice were allowed to sleep, and had no detrimental effect on memory. Neither SD schedule impaired object familiarity processing, suggesting that only specific cognitive abilities were sensitive to the intervention. Sleep may either actively promote memory formation, or alternatively, sleep may provide optimal conditions of non-interference for consolidation.

Adrenocorticotropic Hormone↗

PubMed2004

Sleep inertia: performance changes after sleep, rest and active waking.

Napping benefits and sustains subsequent performance. Prophylactic naps have been recommended as a means to maintain performance during extended wakefulness, as required during shiftwork. However, napping may cause short-term performance impairments, because awakening from sleep is followed by sleep inertia, a period of hypovigilance and impaired cognitive and behavioral performance. We investigated sleep inertia after an afternoon nap. Healthy 18-28 year-olds (n=50, not sleep deprived) were assigned to sleep, active wake or rest groups for a 2-h experimental phase with polysomnography starting either at 14:00 or 16:00 for half of each group. Before (baseline, 12:30 or 14:30) and in five sessions during the hour after the experimental phase (16:00-17:00 or 18:00-19:00), subjects completed an addition task, an auditory reaction time task, and the Stanford Sleepiness Scale. In session one, addition speed in the sleep group was reduced compared with baseline and with active wake controls, whereas calculation accuracy did not change. Addition speed in the sleep and rest groups increased substantially from session one to session two and reached a level similar to that of the active wake group by the fifth session. In the first session, auditory reaction speed of the sleep group was reduced compared with baseline and with rest controls but did not differ from the active wake group. The slowest reaction times showed significant recovery after 20 min. The groups reported similar increases in subjective sleepiness after the experimental period. These findings provide evidence for performance slowing and recovery during the hour following a 2-h nap opportunity. They highlight the importance of employing multiple control groups and various objective and subjective measures to assess sleep inertia.

Acoustic Stimulation↗

PubMed2003

Inhibitory control of intrinsic hippocampal oscillations?

An oscillatory mode of activity is a basic operational mode of the hippocampus. Such activity involves the concurrent expression of several rhythmic processes, of which theta (4-15 Hz) and gamma (20-80 Hz) oscillations are prominent and considered to be important for cognitive processing. In an experimental model that preserves the intrinsic network oscillator, exhibiting the dependency on cholinergic inputs and consequent expression of concurrent theta and gamma oscillations, we investigate the intrinsic mechanisms underlying such integrated hippocampal network responses. This experimental framework is used here to examine the currently prevailing dogma, that interneurons control hippocampal oscillations. The spontaneous response of individual pyramidal cells (in areas CA3 and CA1) and interneurons (area CA3), during oscillatory activity, was monitored intracellularly. Particular attention was given to the initiation of interneuron discharge during oscillations, to the impact of the synaptic output of discharging interneurons on the oscillatory activity, and to the time at which interneurons discharge in relation to the oscillatory cycles. Analysis of the spontaneous patterns of activity in individual interneurons and their outcome, during the oscillatory activity, revealed that interneuron activity is incompatible with initiating, pacing or determining the oscillatory frequencies, although contributing to the apparent rhythmic patterns. Moreover, our results show that non-interneuronal members of the network control interneuron activity. We therefore suggest that the activity of the excitatory cells, i.e., principle cells, is critical toward the initiation, pacing and synchronization of intrinsic hippocampal network oscillations.

Animals↗