1,721,017 research outputs found
Sleep as a behavioral model of neuro-immune interactions
No full textThe central nervous system, by a variety of mechanisms engages in constant surveillance of the peripheral immune system. Alterations in the status of the peripheral immune system induced by an invading pathogen for example, are quickly detected by the central nervous system, which then responds by altering physiological processes and behavior in an attempt to support the immune system in its efforts to eliminate the pathogen. Sleep is one of several behaviors that are dramatically altered in response to infection. Immune-active substances such as the pro-inflammatory cytokines interleukin-1 and tumor necrosis factor, either directly or indirectly via interactions with neurotransmitters or neurohormones are involved in the regulation of sleep. Because these cytokines increase during infection, they are likely candidates for mediating the profound alterations in sleep that occur during infection. Since regulation of behavior is the function of the central nervous system, infection-induced alterations in behavior provide a unique model for the study of neuro-immune interactions
Cytokine-neurotransmitter interactions in the brain
No full textThe data reviewed in this study show that immune-active molecules, such as infectious agents and their components, and cytokines, may induce profound alterations in several neurotransmitters in the CNS. The activation of the immune system elicits fever, behavioral and neuroendocrine changes and may be involved in neuropathological changes occurring in CNS conditions. These effects may be achieved through and accounted for by the changes induced in central neurotransmitters and in the neuroendocrine system by immune challenges. The present review will summarize the available evidence of the reciprocal interactions between cytokines and neurotransmitters in the CNS
How (and why) the immune system makes us sleep
Full text linkGood sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value
AN IL-1 RECEPTOR AND AN IL-1 RECEPTOR ANTAGONIST ATTENUATE MURAMYL DIPEPTIDE- AND IL-1-INDUCED SLEEP AND FEVER
No full textIt is hypothesized that the somnogenic and pyrogenic effects of muramyl dipeptide (MDP) are mediated via enhanced interleukin-1 (IL-1) production. To test this hypothesis the effects of intracerebroventricular (icv) administration of a recombinant human soluble type I IL-1 receptor (sIL-1r) and of the IL-1 receptor antagonist (IL-1ra) on MDP-induced sleep and fever were evaluated in rabbits. The sIL-1r recognized rabbit IL-1beta, but it did not affect sleep or brain temperature across the dose range tested (1-50 mug) when injected icv into normal rabbits. Pretreatment of rabbits with 50 mug sIL-1r or 10 mug IL-1ra blocked human recombinant IL-1-enhanced non-rapid eye movement (NREM) sleep and fever. Thus both the sIL-1r and the IL-1ra were effective antagonists of IL-1 actions. When the animals were pretreated with either 50 mug sIL-1r or with 10 or 100 mug of the IL-1ra, the somnogenic effects of 150 pmol MDP were attenuated. However, the sIL-1r had little effect on MDP-induced febrile responses. These results suggest that the sIL-1r and the IL-1ra can function as antagonists of IL-1 actions in vivo and that MDP-induced sleep and fever are partially mediated by IL-1
Hippocampal type 1 (movement-related) theta rhythm positively correlates with serotonergic activity
No full textTo investigate the relationship between the hippocampal υ activity (or Rhythmical Slow Activity, RSA) and the hippocampal serotonergic activity during spontaneous behavior, simultaneous recordings of i) hippocampal EEG, ii) sleepwake activity, and iii) hippocampal levels of the serotonin (5-HT) metabolite 5-hydroxyndolacetic acid (5-HIAA - measured by in vivo voltammetry and infrared telemetry) were performed. The results show that hippocampal type 1 RSA recorded during wakefulness and voluntary movements (such as walking), is positively correlated to hippocampal 5-HIAA levels. Since in the experimental conditions used in the study, 5-HIAA levels are a reliable index of 5-HT release, the results support the hypothesis that hippocampal type 1 RSA is generated by a serotonergic mechanism. In contrast, hippocampal type 2 RSA recorded during desynchronized sleep is negatively correlated with 5-HT release, suggesting a different neurochemical mechanism for its production. These results also show that, in the experimental condition of this study, hippocampal RSA power spectrum has a main peak frequency of 3.5 during wakefulness, and of 6.5 Hz during desynchronized sleep
Inhibition of caspase-1 in rat brain reduces spontaneous nonrapid eye movement sleep and nonrapid eye movement sleep enhancement induced by lipopolysaccharide
No full textEvidence suggests that IL-1beta is involved in promoting physiol. nonrapid eye movement (NREM) sleep. IL-1beta has also been proposed to mediate NREM sleep enhancement induced by bacteria or their components. Mature and biologically active IL-1beta is cleaved from an inactive precursor by a cysteinyl aspartate-specific protease (caspase)-1. This study aimed to test the hypothesis that inhibition in brain of the cleavage of biol. active IL-1beta will reduce in rats both spontaneous NREM sleep and NREM sleep enhancement induced by the peripheral administration of components of the bacterial cell wall. To test this hypothesis, rats were intracerebroventricularly administered the caspase-1 inhibitor Ac-Tyr-Val-Ala-Asp chloromethyl ketone (YVAD; 3, 30, 300, and 1,500 ng) or were pretreated intracerebroventricularly with YVAD (300 ng) and then i.p. injected with the gram-neg. bacterial cell wall component LPS (250 mg/kg). Subsequent sleep-wake behavior was detd. by std. polygraphic recordings. YVAD administration at the beginning of the light phase of the light-dark cycle significantly reduced time spontaneously spent in NREM sleep during the first 12 postinjection hours. YVAD pretreatment also completely prevented NREM sleep enhancement induced by peripheral LPS administration at the beginning of the dark phase. These results, in agreement with previous evidence, support the involvement of brain IL-1beta in physiol.ogical promotion of NREM sleep and in mediating NREM sleep enhancement induced by peripheral immune challenge
CHANGES IN SPONTANEOUS ACTIVITY OF MEDIALIS DORSALIS THALAMIC NEURONS DURING SLEEP AND WAKEFULNESS
No full textIn chronic unanaesthetized cats unitary activity of medialis dorsalis (MD) thalamic neurones was recorded during wakefulness (W), slow wave (SWS) and desynchronized (DS) sleep. The discharge pattern of these neurones changes during SWS compared to W. Comparison between desynchronization of W and DS shows a change in the mean frequency, being higher in W than in DS. The results suggest that MD neurones participate in the organization of the sleep-wakefulness cycle
CHANGES IN SLEEP WAKING CYCLE INDUCED BY LESIONS OF MEDIALIS DORSALIS THALAMIC NUCLEI IN THE CAT
No full textBilateral lesions of medialis dorsalis (MD) thalamic nuclei in chronically implanted cats disrupt the sleep-waking cycle by inducing a reduction of both slow-wave and desynchronized sleep and a corresponding increase of wakefulness. Bilateral lesions of the anterior thalamic group produce some postural deficits but no changes in the percentage of sleep and wakefulness. The hypothesis that MD lesions alter the sleep processes by interrupting an anterior forebrain-MD-cortical link has been put forward
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