Temporal exposure to chronic unpredictable stress induces precocious neurobehavioral deficits by distorting neuromorphology and glutathione biosynthesis in zebrafish brain

2021 ◽  
pp. 113672
Author(s):  
Lilesh Kumar Pradhan ◽  
Pradyumna Kumar Sahoo ◽  
Nishant Ranjan Chauhan ◽  
Saroj Kumar Das
SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.


Redox Biology ◽  
2021 ◽  
Vol 43 ◽  
pp. 101993
Author(s):  
Xupeng Bai ◽  
Jie Ni ◽  
Julia Beretov ◽  
Valerie C. Wasinger ◽  
Shanping Wang ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 637
Author(s):  
Nicholas S. Moore ◽  
Robert A. Mans ◽  
Mackenzee K. McCauley ◽  
Colton S. Allgood ◽  
Keri A. Barksdale

Evidence from human and animal studies indicate that disrupted light cycles leads to alterations of the sleep state, poor cognition, and the risk of developing neuroinflammatory and generalized health disorders. Zebrafish exhibit a diurnal circadian rhythm and are an increasingly popular model in studies of neurophysiology and neuropathophysiology. Here, we investigate the effect of alterations in light cycle on the adult zebrafish brain: we measured the effect of altered, unpredictable light exposure in adult zebrafish telencephalon, homologous to mammalian hippocampus, and the optic tectum, a significant visual processing center with extensive telencephalon connections. The expression of heat shock protein-70 (HSP70), an important cell stress mediator, was significantly decreased in optic tectum of adult zebrafish brain following four days of altered light exposure. Further, pSer473-Akt (protein kinase B) was significantly reduced in telencephalon following light cycle alteration, and pSer9-GSK3β (glycogen synthase kinase-3β) was significantly reduced in both the telencephalon and optic tectum of light-altered fish. Animals exposed to five minutes of environmental enrichment showed significant increase in pSer473Akt, which was significantly attenuated by four days of altered light exposure. These data show for the first time that unpredictable light exposure alters HSP70 expression and dysregulates Akt-GSK3β signaling in the adult zebrafish brain.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Adèle Weber Zendrera ◽  
Nataliya Sokolovska ◽  
Hédi A. Soula

AbstractIn this manuscript, we propose a novel approach to assess relationships between environment and metabolic networks. We used a comprehensive dataset of more than 5000 prokaryotic species from which we derived the metabolic networks. We compute the scope from the reconstructed graphs, which is the set of all metabolites and reactions that can potentially be synthesized when provided with external metabolites. We show using machine learning techniques that the scope is an excellent predictor of taxonomic and environmental variables, namely growth temperature, oxygen tolerance, and habitat. In the literature, metabolites and pathways are rarely used to discriminate species. We make use of the scope underlying structure—metabolites and pathways—to construct the predictive models, giving additional information on the important metabolic pathways needed to discriminate the species, which is often absent in other metabolic network properties. For example, in the particular case of growth temperature, glutathione biosynthesis pathways are specific to species growing in cold environments, whereas tungsten metabolism is specific to species in warm environments, as was hinted in current literature. From a machine learning perspective, the scope is able to reduce the dimension of our data, and can thus be considered as an interpretable graph embedding.


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