Autochthonous intestinal bacteria and coprophagy: A possible contribution to the ontogeny and rhythmicity of Slow Wave Sleep in mammals.

Brown, Richard A.; Price, Rhelma J.; King, Maurice G.; Husband, Alan J.

doi:10.1016/0306-9877(88)90096-5

Cited by 10 publications

(2 citation statements)

References 19 publications

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“…In the late 1980s and early 1990s a team at the University of Newcastle in Australia were working on slow wave sleep and sleep disturbances, where they had generated a series of solid publications [10][11][12]. By the early 1990's they had biochemically fractionated blood to identify a bioactive peptide.…”

Section: Pgrmc and The Gut Its Microbiota And Metabolic Controlmentioning

confidence: 99%

Quo vadis PGRMC? Grand-Scale Biology in Human Health and Disease

Cahill

2022

Front. Biosci. (Landmark Ed)

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The title usage of Latin Quo vadis 'where are you going' extends the question Unde venisti from where 'did you come?' posed in the accompanying paper and extends consideration of how ancient eukaryotic and eumetazoan functions of progesterone receptor membrane component (PGRMC) proteins (PGRMC1 and PGRMC2 in mammals) could influence modern human health and disease. This paper attempts to extrapolate to modern biology in terms of extensions of hypothetical ancestral functional states from early eukaryotes and the last eumetazoan common ancestor (LEUMCA), to relativize human metabolic physiology and disease. As novel cell types and functional specializations appeared in bilaterian animals, PGRMC functions are hypothesized to have continued to be part of the toolkit used to develop new cell types and manage increasingly complex tasks such as nerve-gut-microbiome neuronal and hormonal communication. A critical role of PGRMC (as one component of a new eumetazoan genetic machinery) is proposed in LEUMCA endocrinology, neurogenesis, and nerve-gut communication with possible involvement in circadian nicotinamide adenine dinucleotide synthesis. This model would explain the contribution of PGRMC to metabolic and differentiation/behavioral changes observed in age-related diseases like diabetes, cancer and perhaps aging itself. Consistent with proposed key regulation of neurogenesis in the LEUMCA, it is argued that Alzheimer's disease is the modern pathology that most closely reflects the suite of functions related to PGRMC biology, with the 'usual suspect' pathologies possibly being downstream of PGRMC1. Hopefully, these thoughts help to signpost directions for future research.

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Section: Pgrmc and The Gut Its Microbiota And Metabolic Controlmentioning

confidence: 99%

Quo vadis PGRMC? Grand-Scale Biology in Human Health and Disease

Cahill

2022

Front. Biosci. (Landmark Ed)

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“…It has been proposed that the commensal gut microflora may serve as a quasiendogenous pool of these somnogenic BCWCs given their quantity and close proximity to the intestinal portal (Brown, 1995;Krueger et al, 1985). A relationship between coprophagy, bacterial colonization of the neonatal gastrointestinal tract, and the ontogeny of SWS and hematopoiesis has also been proposed (Brown et al, 1988;Korth et al, 1995). If proven correct, similar to essential amino acids and vitamins, BCWCs may be an exogenous requirement for normal physiological processes, in this case for the upkeep of host defense mechanisms and for the generation of SWS (Krueger & Karnovsky, 1995).…”

Section: Introductionmentioning

confidence: 99%

Sleep and the gut microbiome: antibiotic-induced depletion of the gut microbiota reduces nocturnal sleep in mice

Lendrum

Seebach

Klein

et al. 2017

Preprint

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Highlights-14 d broad-spectrum antibiotic treatment effectively depletes the gut microbiota.-Gut microbiota depletion reduces nocturnal sleep, but not diurnal sleep.-Gut microbiota depletion increases nocturnal locomotion, but not diurnal locomotion.-Antibiotics may be insomnogenic: implications for idiopathic sleep disorders. AbstractSeveral bacterial cell wall components such as peptidoglycan and muramyl peptide are potent inducers of mammalian slow-wave sleep when exogenously administered to freely behaving animals. It has been proposed that the native gut microflora may serve as a quasi-endogenous pool of somnogenic bacterial cell wall products given their quantity and close proximity to the intestinal portal. This proposal suggests that deliberate manipulation of the host's intestinal flora may elicit changes in host sleep behavior. To test this possibility, we evaluated 24 h of sleep-wake behavior after depleting the gut microbiota with a 14 d broad-spectrum antibiotic regimen containing high doses of ampicillin, metronidazole, neomycin, and vancomycin. Highthroughput sequencing of the bacterial 16S rDNA gene was used to confirm depletion of fecal bacteria and sleep-wake vigilance states were determined using videosomnography techniques based on previously established behavioral criteria shown to highly correlate with standard polysomnography-based methods. Additionally, considering that germ-free and antibiotic-treated mice have been earlier shown to display increased locomotor activity, and since locomotor activity has been used as a reliable proxy of sleep, we suspected that the elevated locomotor activity previously . CC-BY 4.0 International license peer-reviewed) is the author/funder. It is made available under aThe copyright holder for this preprint (which was not . http://dx.doi.org/10.1101/199075 doi: bioRxiv preprint first posted online Oct. 5, 2017; reported in these animals may reflect an unreported reduction in sleep behavior. To examine this potential relationship, we also quantified locomotor activity on a representative subsample of the same 24 h of video recordings using the automated video-tracking software ANY-maze. We found that antibiotic-induced depletion of the gut microbiota reduced nocturnal sleep, but not diurnal sleep. Likewise, antibiotictreated mice showed increased nocturnal locomotor activity, but not diurnal locomotor activity. Taken together, these results support a link between the gut microbiome and nocturnal sleep and locomotor physiology in adult mice. Additionally, our findings indicate that antibiotics may be insomnogenic via their ability to diminish gut-derived bacterial somnogens. Given that antibiotics are among the most commonly prescribed drugs in human medicine, these findings have important implications for clinical practice with respect to prolonged antibiotic therapy, insomnia, and other idiopathic sleep-wake and circadian-rhythm disorders affecting an estimated 50-70 million people in the United States alone.

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Autochthonous intestinal bacteria and coprophagy: A possible contribution to the ontogeny and rhythmicity of Slow Wave Sleep in mammals.

Cited by 10 publications

References 19 publications

Quo vadis PGRMC? Grand-Scale Biology in Human Health and Disease

Quo vadis PGRMC? Grand-Scale Biology in Human Health and Disease

Sleep and the gut microbiome: antibiotic-induced depletion of the gut microbiota reduces nocturnal sleep in mice

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