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Biomedical subjects

Maurizio Mariotti

Publications and source records attributed to Maurizio Mariotti.

4 recordsLinked to original sources

Sleep, but not febrile responses of Fisher 344 rats to immune challenge are affected by aging.

Sleep is altered in response to infection and immune challenge in humans and non-human animals. Although there are changes in sleep and facets of immune function with aging, sleep responses of aged subjects to immune challenge have received little, if any attention. To test the hypothesis that aging affects sleep responses to immune challenge, intracerebroventricular injections of interleukin 1 (IL-1) were given to young and aged rats and subsequent sleep-wake behavior was determined. Under basal conditions and in the absence of an immune challenge, sleep patterns of young (3 months) and aged (25-27 months) Fisher 344 rats did not differ. In young animals, IL-1 (2.5 ng) enhanced non-rapid eye movement (NREM) sleep, inhibited rapid eye movement (REM) sleep, and induced fever. In aged animals, IL-1 administration did not alter NREM sleep, but REM sleep was inhibited and brain temperature increased to the same extent observed in young animals. These results show that alterations in sleep following immune challenge are impacted by aging, whereas febrile responses are not. Since it has been postulated that enhanced NREM sleep may facilitate recovery from microbial infection, the present results also suggest that the lack of NREM sleep responses of aged rats to immune challenge may contribute to the increased infection-induced morbidity and mortality of aged organisms.

Aging↗

Interleukin-1beta enhances non-rapid eye movement sleep when microinjected into the dorsal raphe nucleus and inhibits serotonergic neurons in vitro.

Interleukin-1 (IL-1) and IL-1 receptors are constitutively expressed in normal brain. IL-1 increases non-rapid eye movements (NREM) sleep in several animal species, an effect mediated in part by interactions with the serotonergic system. The site(s) in brain at which interactions between IL-1 and the serotonergic system increase NREM sleep remain to be identified. The dorsal raphe (DRN) is the origin of the major ascending serotonergic pathways to the forebrain, and it contains IL-1 receptors. This study examined the hypothesis that IL-1 increases NREM sleep by acting at the level of the DRN. IL-1beta (0.25 and 0.5 ng) was microinjected into the DRN of freely behaving rats and subsequent effects on sleep-wake activity were determined. IL-1beta 0.5 ng increased NREM sleep during the first 2 h post-injection from 33.5 +/- 3.7% after vehicle microinjection to 42.9 +/- 3.0% of recording time. To determine the effects of IL-1beta on electrophysiological properties of DRN serotonergic neurons, intracellular recordings were performed in a guinea-pig brain stem slice preparation. In 26 of 32 physiologically and pharmacologically identified serotonergic neurons, IL-1beta superfusion (25 ng/mL) decreased spontaneous firing rates by 50%, from 1.6 +/- 0.2 Hz (before IL-1beta superfusion) to 0.8 +/- 0.2 Hz. This effect was reversible upon washout. These results show that IL-1beta increases NREM sleep when administered directly into the DRN. Serotonin enhances wakefulness and these novel data also suggest that IL-1beta-induced enhancement of NREM sleep could be due in part to the inhibition of DRN serotonergic neurons.

Action Potentials↗

EEG slow (approximately 1 Hz) waves are associated with nonstationarity of thalamo-cortical sensory processing in the sleeping human.

Intracellular studies reveal that, during slow wave sleep (SWS), the entire cortical network can swing rhythmically between extremely different microstates, ranging from wakefulness-like network activation to functional disconnection in the space of a few hundred milliseconds. This alternation of states also involves the thalamic neurons and is reflected in the EEG by a slow (<1 Hz) oscillation. These rhythmic changes, occurring in the thalamo-cortical circuits during SWS, may have relevant, phasic effects on the transmission and processing of sensory information. However, brain reactivity to sensory stimuli, during SWS, has traditionally been studied by means of sequential averaging, a procedure that necessarily masks any short-term fluctuation of responsiveness. The aim of this study was to provide a dynamic evaluation of brain reactivity to sensory stimuli in naturally sleeping humans. To this aim, single-trial somatosensory evoked potentials (SEPs) were grouped and averaged as a function of the phase of the ongoing sleep slow (<1 Hz) oscillation. This procedure revealed a dynamic profile of responsiveness, which was conditioned by the phase of the spontaneous sleep EEG. Overall, the amplitude of the evoked potential changed sistematically, increasing and approaching wakefulness levels along the negative slope of the EEG oscillation and decaying below SWS average levels along the positive drift. These marked and fast changes of stimulus-correlated electrical activity involved both short (N20) and long latency (P60 and P100) components of SEPs. In addition, the observed short-term response variability appeared to be centrally generated and specifically related to the evolution of the spontaneous oscillatory pattern. The present findings demonstrate that thalamo-cortical processing of sensory information is not stationary in the very short period (approximately 500 ms) during natural SWS.

Cerebral Cortex↗

Awakening from sleep.

Awakening is a crucial event for the organism. The transition from sleep to waking implies physiological processes which lead to a new behavioural state. Spontaneous awakenings have varying features which may change as a function of several factors. The latter include intrasleep architecture, circadian phase, time awake, age, or disordered sleep. Despite its clear theoretical and clinical importance, the topic of awakening (in humans) has received little attention so far. This contribution focuses on major issues which relate to awakening from both basic (experimental) and clinical research. Recent knowledge on neurophysiological mechanisms is reported. The experimental data which provide in the human suggestions on the regulation of awakening are discussed, mainly those concerning sleep architecture and homeostatic/circadian factors also in a life-span perspective, since age is a powerful factor which may influence awakening. Clinical contributions will examine two main sleep disorders: insomnia and hypersomnia. Daytime functioning is shown in insomniac patients and compared to other pathologies like sleep apnea. A final section evokes links between some types of night waking and psychological factors.

Adrenocorticotropic Hormone↗