Secretions from placenta, after hypoxia/reoxygenation, can damage developing neurones of brain under experimental conditions

Curtis, Daniel; Sood, Anubhuti; Phillips, Tom J.; Leinster, Veronica H.L.; Nishiguchi, Akihiro; Coyle, Clare; Lacharme-Lora, Lizeth; Beaumont, Oliver; Kemp, Helena; Goodall, Roberta; Cornes, Leila; Giugliano, Michèle; Barone, Rocco A; Matsusaki, Michiya; Akashi, Mitsuru; Tanaka, Hiroyoshi; Kano, Mitsunobu R.; McGarvey, Jennifer C.; Halemani, Nagaraj D.; Simon, Katja; Keehan, R.; Ind, William; Masters, Tracey; Grant, Simon; Athwal, Sharan; Collett, Gavin; Tannetta, Dionne; Sargent, Ian L.; Scull-Brown, Emma; Liu, Xun; Aquilina, Kristian; Cohen, Nicki; Lane, Jon D.; Thoresen, Marianne; Hanley, Jonathan G.; Randall, Andrew D.; Case, C. P.

doi:10.1016/j.expneurol.2014.05.003

Cited by 34 publications

(36 citation statements)

References 52 publications

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“…If our lady urbanite is pregnant, then air pollutant components can cross the placental barrier, directly affecting the embryo and the fetus [23,24]. Continuous expression of potent inflammatory mediators in the CNS and the formation of reactive oxygen species (ROS) are major findings in urban residents.…”

Section: Neuroinflammatory and Neurodegenerative Changesmentioning

confidence: 99%

“…Longitudinal birth cohort studies on chronic early life pollutant exposures, bring up the issue of the critical importance of prenatal exposures and the role of the placental barrier in the final brain effects on the fetus. Curtis et al, identified glutamate as the active factor release from the placenta/cytotrophoblast barriers in vitro after hypoxia or hypoxia/reoxygenation, capable of damaging developing neurons under experimental conditions [23]. Thus, additional factors to consider would be the placental damage by the culprit air pollutant and the resulting release factors damaging the developing brain, functionally effective tight junctions present in embryonic brain, specific transport of plasma proteins across the blood-CSF barrier and embryo-specific intercellular junctions between neuroependymal cells lining the ventricles [24].…”

Section: Cognition Effects and Brain Structural Changesmentioning

confidence: 99%

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Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

et al. 2016

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Air pollution (indoor and outdoor air) is a major issue in public health as epidemiological studies haven pointed to the numerous detrimental health consequences (notably, respiratory and cardiovascular pathology). In the last fifteen years, air pollution has also been considered as a potent environmental risk factor for neurological diseases and neuropathology. In this review, the authors examine the impact of air pollution on children's brain development and its clinical, cognitive, brain structural and metabolic consequences. Long-term potential consequences for adults' brain and effects on multiple sclerosis are also discussed. One challenge is assessing lifetime exposures to outdoor and indoor environments, including occupational exposures: how much, for how long and what type. The diffuse neuroinflammation, the damage to the neurovascular unit, and the production of auto-antibodies to neural and tight junction proteins are worrisome findings in children chronically exposed to concentrations above current standards for ozone and fine particulate matter (PM 2.5 ) and may constitute significant risk factors for the development of Article Outline

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Section: Neuroinflammatory and Neurodegenerative Changesmentioning

confidence: 99%

Section: Cognition Effects and Brain Structural Changesmentioning

confidence: 99%

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

et al. 2016

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“…Previous research has suggested that the placenta, as the interface between mother and foetus, plays a key role in neurodevelopment and in foetal programming of psychological disorders that result from adverse events during pregnancy 31,40,41 . In keeping with this concept, the results presented here demonstrate for the first time that maternal exposure to social stress during pregnancy induces oxidative stress in the placenta, highlighting the potential significance of the placenta in mediating the effects of social stress on the offspring.…”

Section: Discussionmentioning

confidence: 99%

“…However, the above suggests that in response to maternal social stress the placenta secretes molecules into the foetal circulation that can alter the foetal brain. We have previously proposed that the placental barrier may respond to a variety of physiological insults by secreting factors that can damage cells distal to the barrier, both in vitro and in vivo, thereby having the potential to play a role in foetal development 31,40,41,66,67 . The current work further supports the hypothesis that factors released from the placenta may mediate the effects of maternal insults during pregnancy on the developing foetal brain.…”

Section: Discussionmentioning

confidence: 99%

“…Cortical cultures were prepared from dissociated rat embryonic day 18 cortical tissue and grown on glass coverslips as described previously 40 , in neuronal culture medium (see above). Placental conditioned medium or foetal plasma (n = 3, each replicate originating from a different dam; collected in Experiment 1) was applied to the cortical cultures for 6 days starting from day 12 in vitro.…”

Section: Cortical Culturesmentioning

confidence: 99%

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Maternal antioxidant treatment prevents behavioural and neural changes in offspring exposed to prenatal social stress

Scott

Phillips

Sze

et al. 2019

Preprint

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Maternal exposure to social stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. However, the mechanism through which the effects of maternal stress are transmitted to the foetus is unclear. Using a rat model, we explored the mechanisms by which maternal social stress is conveyed to the foetus and the potential for targeted treatment to prevent disease in the offspring. Maternal stress increased circulating corticosterone in the mother, but not the foetuses. Maternal stress also induced oxidative stress in the placenta, but not in the foetal brain, and this was prevented by administration of a nanoparticle-bound antioxidant. Moreover, antioxidant treatment prevented prenatal stress-induced anxiety-like behaviour in the adult male offspring, along with several stress-induced neuroanatomical, neurochemical and gene expression changes in the offspring brain. Importantly, many of these neural effects were mimicked in neuronal cultures by application of placental-conditioned medium or foetal plasma from stressed pregnancies.Both placental-conditioned medium and foetal plasma contained differentially abundant extracellular microRNAs following prenatal stress. The present study highlights the crucial role of the placenta, and the molecules it secretes, in foetal brain development and provides evidence of the potential for treatment that can prevent maternal stress-induced foetal programming of neurological disease.

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Transient sublethal hypoxia in neonatal rats causes reduced dendritic spines, aberrant synaptic plasticity, and impairments in memory

Tang

Xin

O’Connor

et al. 2020

J of Neuroscience Research

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Hypoxic/ischemic insult, a leading cause of functional brain defects, has been extensively studied in both clinical and experimental animal research, including its etiology, neuropathogenesis, and pharmacological interventions. Transient sublethal hypoxia (TSH) is a common clinical occurrence in the perinatal period. However, its effect on early developing brains remains poorly understood. The present study was designed to investigate the effect of TSH on the dendrite and dendritic spine formation, neuronal and synaptic activity, and cognitive behavior of early postnatal Day 1 rat pups. While TSH showed no obvious effect on gross brain morphology, neuron cell density, or glial activation in the hippocampus, we found transient hypoxia did cause significant changes in neuronal structure and function. In brains exposed to TSH, hippocampal neurons developed shorter and thinner dendrites, with decreased dendritic spine density, and reduced strength in excitatory synaptic transmission. Moreover, TSH‐treated rats showed impaired cognitive performance in spatial learning and memory. Our findings demonstrate that TSH in newborn rats can cause significant impairments in synaptic formation and function, and long‐lasting brain functional deficits. Therefore, this study provides a useful animal model for the study of TSH on early developing brains and to explore potential pharmaceutical interventions for patients subjected to TSH insult.

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Secretions from placenta, after hypoxia/reoxygenation, can damage developing neurones of brain under experimental conditions

Cited by 34 publications

References 52 publications

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

Maternal antioxidant treatment prevents behavioural and neural changes in offspring exposed to prenatal social stress

Transient sublethal hypoxia in neonatal rats causes reduced dendritic spines, aberrant synaptic plasticity, and impairments in memory

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