Circadian cycle-dependent EEG biomarkers of pathogenicity in adult mice following prenatal exposure to in utero inflammation

Adler, Daniel A; Ammanuel, Simon; Lei, Jun; Dada, Tahani; Borbiev, Talaibek; Johnston, Michael V.; Kadam, Shilpa D.; Burd, Irina

doi:10.1016/j.neuroscience.2014.06.022

Cited by 23 publications

(18 citation statements)

References 39 publications

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“…No significance was found between treatment groups for the delta power data; however, significant activity-dependent changes in theta-beta power ratios seen in controls were absent in the LPS-exposed mice. In conclusion, exposure to in utero inflammation in CD1 mice resulted in significantly altered sleep architecture as adults that were circadian cycle and activity state dependent (Adler, Ammanuel et al 2014).…”

Section: Animal Modelsmentioning

confidence: 85%

“…Intrauterine infection or inflammation in preterm neonates is a known risk for adverse neurological outcomes, including cognitive, motor, and behavioral disabilities (Adler et al, 2014). Our previous data suggest that there is acute fetal brain inflammation in a mouse model of intrauterine exposure to LPS.…”

Section: Animal Modelsmentioning

confidence: 87%

“…During this period, NREM and REM sleep of rats increases during the dark period, whereas these sleep phases are reduced during the light period. Analyses of EEG power spectrums for delta and theta-beta power ratios during wake vs sleep cycles further show that LPS-exposed mice evidence alterations in theta-beta power ratios that are circadian cycle and activity state dependent (Adler et al, 2014).…”

Section: Animal Modelsmentioning

confidence: 96%

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Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Irwin

Opp

2016

Neuropsychopharmacol

361

268

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Sleep disturbances including insomnia independently contribute to risk of inflammatory disorders and major depressive disorder. This review and overview provides an integrated understanding of the reciprocal relationships between sleep and the innate immune system and considers the role of sleep in the nocturnal regulation of the inflammatory biology dynamics; the impact of insomnia complaints, extremes of sleep duration, and experimental sleep deprivation on genomic, cellular, and systemic markers of inflammation; and the influence of sleep complaints and insomnia on inflammaging and molecular processes of cellular aging. Clinical implications of this research include discussion of the contribution of sleep disturbance to depression and especially inflammation-related depressive symptoms. Reciprocal action of inflammatory mediators on the homeostatic regulation of sleep continuity and sleep macrostructure, and the potential of interventions that target insomnia to reverse inflammation, are also reviewed. Together, interactions between sleep and inflammatory biology mechanisms underscore the implications of sleep disturbance for inflammatory disease risk, and provide a map to guide the development of treatments that modulate inflammation, improve sleep, and promote sleep health.

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Section: Animal Modelsmentioning

confidence: 85%

Section: Animal Modelsmentioning

confidence: 87%

Section: Animal Modelsmentioning

confidence: 96%

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Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Irwin

Opp

2016

Neuropsychopharmacol

361

268

View full text Add to dashboard Cite

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“…In the present study, it could be possible that a fluctuating level of anesthesia, instead of the subject’s sleep state, could have contributed to the greater variability of FC. Alternatively, rapid fluctuation between awake and sleep states in mice (Adler et al 2014) could have contributed to the greater variability of FC compared to humans. According to the results of the analysis using power spectra (Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

Neuronal origin of the temporal dynamics of spontaneous BOLD activity correlation

Matsui

Murakami

Ohki

2017

Preprint

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(199/200 words)2 0Resting-state functional connectivity (FC) has become a major fMRI method to study dynamics of calcium FC and hemodynamic FC measured in the same short time windows.3 0Moreover, we found that variation in transient neuronal coactivation patterns (CAPs) wassignificantly related to temporal fluctuations of sliding window FC in hemodynamics. 2Finally, we show that the observed dynamics of FC cannot be fully accounted for by temporally sparse events that can be extracted using a small number of time points.

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“…We believe that these changes in cytokine profile were associated with MSC interaction with dendritic cells. 81 It is known that, in addition to inhibitory effects in macrophages, MSCs may exert promoting effects on lipopolysaccharide-induced dendritic cells. 82 Ultimately, the shift in cytokine profile allowed for decreases in detrimental maternal and fetal phenotypes.…”

Section: Commentmentioning

confidence: 99%

Murine model: maternal administration of stem cells for prevention of prematurity

Lei

Firdaus

Rosenzweig

et al. 2015

American Journal of Obstetrics and Gynecology

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OBJECTIVE Using a mouse model of intrauterine inflammation, we have demonstrated that exposure to inflammation induces preterm birth and perinatal brain injury. Mesenchymal stem cells (MSCs) have been shown to exhibit immunomodulatory effects in many inflammatory conditions. We hypothesized that treatment with human adipose tissue-derived MSCs may decrease the rate of preterm birth and perinatal brain injury through changes in antiinflammatory and regulatory milieu. STUDY DESIGN A mouse model of intrauterine inflammation was used with the following groups: (1) control; (2) intrauterine inflammation (lipopolysaccharide); and (3) intrauterine lipopolysaccharide + intraperitoneal (MSCs). Preterm birth was investigated. Luminex multiplex enzyme-linked immunosorbent assays were performed for protein levels of cytokines in maternal and fetal compartments. Immunofluorescent staining was used to identify and localize MSCs and to examine microglial morphologic condition and neurotoxicity in perinatal brain. Behavioral testing was performed at postnatal day 5. RESULTS Pretreatment with MSCs significantly decreased the rate of preterm birth by 21% compared with the lipopolysaccharide group (P < .01). Pretreatment was associated with increased interleukin-10 in maternal serum, increased interleukin-4 in placenta, decreased interleukin-6 in fetal brain (P < .05), decreased microglial activation (P < .05), and decreased fetal neurotoxicity (P < .05). These findings were associated with improved neurobehavioral testing at postnatal day 5 (P < .05). Injected MSCs were localized to placenta. CONCLUSION Maternally administered MSCs appear to modulate maternal and fetal immune response to intrauterine inflammation in the model and decrease preterm birth, perinatal brain injury, and motor deficits in offspring mice.

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Circadian cycle-dependent EEG biomarkers of pathogenicity in adult mice following prenatal exposure to in utero inflammation

Cited by 23 publications

References 39 publications

Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Neuronal origin of the temporal dynamics of spontaneous BOLD activity correlation

Murine model: maternal administration of stem cells for prevention of prematurity

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